Syncope in children with Tourette's syndrome treated with guanfacine.

We report on 4 children who experienced a syncopal episode while being treated with guanfacine without any other evident cause. Syncope appears to be an uncommon side effect of guanfacine and is probably due to drug-induced hypotension or bradycardia.     

Brief review: History, concept and controversies in the neurological determination of death

PURPOSE: Despite general worldwide acceptance of the concept of neurological determination of death (NDD), inconsistencies in clinical criteria and ancillary testing requirements remain. Numerous guidelines for NDD may be applied in clinical practice by a variety of medical practitioners, but the scientific rationale for specific guideline recommendations often remains unclear. This review examines the evolution of NDD, and seeks to provide scientific validation for existing NDD criteria. SOURCE: English language peer-reviewed medical journals and established contemporary medical texts. PRINCIPAL FINDINGS: Currently published guidelines appear to have evolved from the work of the ad hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death. The Conference of the Royal Colleges and Faculties of the United Kingdom refined the criteria and subsequently adopted the principal of brainstem death. While the fundamentals of NDD guidelines are remarkably consistent worldwide, specific criteria and requirements are often inconsistent. CONCLUSION: Numerous controversies regarding NDD continue to exist, necessitating further scientific clarification of these issues. More recently published guidelines representing the collective opinion of world experts in NDD based upon best current scientific evidence are available in current medical journals.     

The Evidence Base Supporting the Subtyping of Gamblers in Treatment

Introduction Recent reviews found problem gamblers are heterogeneous and recommended subtyping gamblers in treatment studies. Objective Review factors (stage of change, preferred gambling activity, co-occurring disorder, and temporal instability of symptoms) for subtyping by evaluating the evidence for their effects on gambling treatment. Methods Literature review, evidence grading. Results Evidence is limited that any of the reviewed factors affects gambling treatment. Substantial evidence from prospective studies and other evidence from cross-sectional studies and the strong placebo response among pathological gamblers support the temporal instability of gambling symptoms. Conclusions Multiple studies are needed to develop the evidence base needed to subtype gamblers in treatment. Changes in the diagnostic criteria of pathological gambling may be necessary, especially to specify the persistence of gambling-related symptoms.     

Additive Effects of Sevoflurane and Propofol on γ-Aminobutyric Acid Receptor Function

Background: Previous studies have shown that propofol and sevoflurane enhance the function of [gamma]-aminobutyric acid type A (GABAA) receptors. However, it is not known whether these two drugs modulate the same molecular pathways. In addition, little is known about receptor function in the presence of both propofol and sevoflurane. The aim of this study was to better understand the interactions of propofol and sevoflurane with the GABAA receptor.

Methods: Wild-type [alpha]1, [beta]2, [gamma]2s GABAA receptor subunit complementary DNAs were transfected into human embryonic kidney cells grown on glass coverslips using a calcium phosphate transfection method. After transfection (36-72 h), cells were whole cell patch clamped and exposed to combinations of the following: 0.3-1,000 [mu]m [gamma]-aminobutyric acid (GABA), 0-10 [mu]m propofol, and 0-1,650 [mu]m sevoflurane. Chemicals were delivered to the cells using two 10-channel infusion pumps and a rapid solution exchanger.

Results: Both propofol and sevoflurane alone enhanced the amplitude of GABAA receptor responses to submaximal concentrations of GABA in a dose-dependent manner. The enhancement was underpinned by an increase in the apparent affinity of the receptor for GABA. Coapplication of both anesthetics further enhanced the apparent affinity of the receptor for GABA.