INTRODUCTION:Torsion of the gallbladder is a rare condition that most commonly affects the elderly. Pre-operative diagnosis is the exception rather than the rule. Any delay in treatment can be fatal as the gallbladder may rupture, leading to biliary peritonitis.CASE PRESENTATION:We present the case of an 80-year-old woman who was admitted with right upper quadrant pain initially thought to be secondary to acute cholecystitis. Subsequent ultrasound and computed tomography scans of the abdomen revealed signs suggestive of acute cholecystitis but neither modality detected any gallstones. As the patient's symptoms failed to resolve on conservative management, she was taken to theatre for an open cholecystectomy. Intra-operatively, the gallbladder had undergone complete torsion and appeared gangrenous. A routine cholecystectomy followed and she recovered from the operation without incident.CONCLUSION:It is rare to diagnose torsion of the gallbladder pre-operatively despite advances in diagnostic imaging. However, this differential diagnosis should be borne in mind particularly in the elderly patient, without proven gallstones, who fails to improve on conservative management. An emergency cholecystectomy is indicated in the event of diagnosing torsion of the gallbladder to avert the potentially lethal sequelae of biliary peritonitis.

Background: In previous studies, depletion of brain serotonin by administration of a tryptophan-free amino acid drink (TFD) (1) temporarily reversed the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) in euthymic patients who had a history of major depression, and (2) enhanced rapid eye movement (REM) sleep in normal volunteers. In this study, we hypothesized that the TFD would not only increase depressive symptoms but also the propensity for REM sleep in euthymic patients treated with SSRIs.Methods: Ten fully remitted, medicated male patients who had a history of major depressive episode ingested a 100-g TFD (the experimental dose) or a 25-g TFD (designed to be the control drink) in double-blind, random order on separate days. The effects were assessed with mood ratings, plasma tryptophan concentrations, and an all-night sleep electroencephalogram.Results: The TFDs produced a dose-dependent reduction in plasma tryptophan concentrations, sleep latency, and REM latency, as well as increased REM percentage, REM minutes, REM density, and total sleep time. Neither strength of TFD altered mood to a clinically significant degree.Conclusions: Although the TFD affected plasma tryptophan concentrations and various sleep measures, our study did not confirm previous reports that TFD temporarily reversed the antidepressant effects of SSRIs in euthymic patients. Our patients however, had been treated for a longer period with SSRIs and were more fully remitted at the time of the study. Our results suggest that TFD-induced relapse in SSRI-treated patients in remission decreases as a function of treatment duration, degree of remission, or both.

Background: To test the hypothesis that depression is associated with art increased ratio of cholinergic to serotonergic neurotransmission, we compared the effects of pilocarpine, a muscarinic agonist, and ipsapirone, a serotonin (5-HT)(1A) agonist, on electroencephalographic (EEG) sleep in depressed and healthy subjects. We hypothesized, adopting the reciprocal interaction model, that the effects on REM sleep of these probes within the same individuals are negatively correlated and unmask neurobiological changes in depression.Methods: Polysomnographic recordings were obtained in 12 unmedicated patients with a current major depression and 12 normal controls. They received placebo, pilocarpine 25 mg, or ipsapirone 10 mg (orally, 15 min before bedtime, after premedication with the peripheral anticholinergic probanthine 30 mg, double blind, counter-balanced) on three occasions.Results: Pilocarpine shortened and ipsapirone prolonged REM latency equally in both groups. These effects were not correlated Pilocarpine decreased slow-wave sleep and EEG delta power during the first nonREM episode more in controls than in patients, and enhanced EEG sigma power equally in both groups. Ipsapirone had no significant effects on EEG power.Conclusion: These data do not support the postulate of muscarinic receptor up-regulation and 5-MT1A receptor down-regulation in depression. The significance of blunted delta power suppression in patients following pilocarpine warrants further investigations. Biol Psychiatry 1998;44: 21-33.

Background: Serotonin has been implicated in the regulation of sleep and mood. In animals a tryptophan-free amino acid drink (TFD) challenge has been found to reduce brain serotonin. We hypothesized this TFD would produce alterations in electroencephalographic (EEG) sleep commonly associated with depression, i.e., an enhancement of rapid eye movement (REM) sleep, and adversely affect mood ratings in humans. Methods: We investigated the effects of a TFD challenge in 11 healthy male subjects on EEG sleep and mood (assessed by Profile of Mood States). All subjects received on separate occasions an experimental drink containing approximately 100 g of an amino acid mixture (100% TFD) and a control drink containing one fourth strength (25% TFD) of the experimental drink 5 hours prior to sleep (6:00 pm). Results: Both drinks significantly decreased plasma tryptophan levels 5 hours postchallenge (11:00 pm). Both drinks significantly decreased REM latency, and the 25% TFD also increased REM time and REM% compared to baseline. No significant changes were found in subjective ratings of depression; however, subjects reported confusion and tension and a decrease in elation, vigor, and friendliness compared with baseline. Conclusions: These TFD findings further support the involvement of serotonin deficiency in EEG sleep findings commonly seen in depression.

The REM sleep-suppressing effect of postsynaptic 5-HT1A stimulation has been well established. Here we investigate the effects of the 5-HT1A agonist ipsapirone (10 and 20 mg) on sleep EEG power spectra during non-REM sleep in nine healthy humans. At the lower dose, slow wave activity (SWA; EEG power in the δ (1–4.5 Hz) range) was significantly enhanced. At the higher dose, where side-effects occurred, the enhancement in SWA was not significant. The spectral profile was characterized by a bimodal increase of power in the lower δ and in the θ (5–8 Hz) frequencies, and by troughs at 4 Hz and at 11 Hz, a pattern compellingly similar to that reported for a 5-HT2 antagonists (seganserin). We propose that the spectral data following the lower ipsapirone dose reflect a net decrease of neuronal activity at 5-HT2 receptors, mediated through stimulation of somatodendritic autoreceptors in the raphe nuclei (presynaptic) and/or through stimulation of postsynaptic 5-HT1A receptors colocalized with 5-HT2 receptors. The spectral non-REM sleep EEG profile might be used to investigate central 5-HT function in humans.