ObjectivesPostoperative hemorrhage is a potentially life-threatening complication in thyroid surgery. This study was performed to review the clinical patterns of post-thyroidectomy hemorrhage, and especially as they are related to the source of bleeding.MethodsWe performed a retrospective review of 10 patients (0.96%) with post-thyroidectomy hemorrhage that required surgical evacuation. The clinical patterns such as the time interval from surgery to hemorrhage and the signs and symptoms according to the bleeding focus were evaluated.ResultsThe mean time interval from surgery to symptom onset was 7 hr 52 min. Six cases showed bleeding deep to the strap muscles, while the other 4 cases showed bleeding superficial to the muscles. Ecchymosis was prominent and dark in color in 3 of the 4 cases (75%) of superficial bleeding, however it was identified in only 2 of the 6 cases (33%) of deep bleeding. Respiratory distress occurred in two cases of hematoma deep to the strap muscles, but in none of the cases with superficial bleeding.ConclusionThe post-thyroidectomy hemorrhage had some different clinical patterns between the superficial cases and the deep cases, showing that life-threatening airway obstruction occurred from the deep hematoma. A thorough understanding of the clinical patterns of post-thyroidectomy hemorrhage between the cases of superficial and those cases of deep hematoma may provide valuable surgical tips to manage this potentially lethal complication.

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Recent studies suggest that ketamine produces antidepressant actions via stimulation of mammalian target of rapamycin (mTOR), leading to increased levels of synaptic proteins in the prefrontal cortex. Thus, mTOR activation may be related to antidepressant action. However, the mTOR signalling underlying antidepressant drug action has not been well investigated. The aim of the present study was to determine whether alterations in mTOR signalling were observed following treatment with antidepressant drugs, using ketamine as a positive control. Using Western blotting, we measured changes in the mTOR-mediated proteins and synaptic proteins in rat hippocampal cultures. Dendritic outgrowth was determined by neurite assay. Our findings demonstrated that escitalopram, paroxetine and tranylcypromine significantly increased levels of phospho-mTOR and its down-stream regulators (phospho-4E-BP-1 and phospho-p70S6K); fluoxetine, sertraline and imipramine had no effect. All drugs tested increased up-stream regulators (phospho-Akt and phospho-ERK) levels. Increased phospho-mTOR induced by escitalopram, paroxetine or tranylcypromine was significantly blocked in the presence of specific PI3K, MEK or mTOR inhibitors, respectively. All drugs tested also increased hippocampal dendritic outgrowth and synaptic proteins levels. The mTOR inhibitor, rapamycin, significantly blocked these effects on escitalopram, paroxetine and tranylcypromine whereas fluoxetine, sertraline and imipramine effects were not affected. The effects of escitalopram, paroxetine and tranylcypromine paralleled those of ketamine. This study presents novel in vitro evidence indicating that some antidepressant drugs promote dendritic outgrowth and increase synaptic protein levels through mTOR signalling; however, other antidepressant drugs seem to act via a different pathway. mTOR signalling may be a promising target for the development of new antidepressant drugs.

The objective of the study was to study the effects of acetylcholinesterase inhibitors on cognition in patients with schizophrenia. We conducted a 12-week, double-blind, placebo-controlled trial of galantamine as adjunctive treatment to conventional antipsychotic drugs on 24 patients with schizophrenia. The 24 patients had been stabilized on conventional antipsychotic drugs (chlorpromazine equivalent dose of 1390 mg/day) for a minimum of 3 months before their enrollment into the study. The patients were evaluated at baseline, and after 6 and 12 weeks using the Korean version of Mini Mental State Examination, Brief Psychiatric Rating Scale, and a standard neuropsychological battery. Compared with placebo, galantamine produced a small and nonsignificant change in the cognitive measures, but the score for recognition on the Rey Complex Figure Test improved significantly in patients given galantamine (P<0.05). Of the several domains of cognitive functions assessed, galantamine tended to improve the score for recognition on the Hopkins Verbal Learning Test and for color on the Stroop Test (P<0.1), but these results were not statistically significant. The scores on the Korean version of Mini Mental State Examination did not change significantly in patients with galantamine, and the psychiatric symptoms did not change. The addition of galantamine to the conventional antipsychotic medication of patients with schizophrenia does not produce a change in the cognitive function or state of psychopathology.