Nationwide survey on the use of image-guided functional endoscopic sinus surgery.

OBJECTIVE: To evaluate impressions and usage of sinus surgery image-guided surgical (IGS) systems by ENT surgeons in the United States. STUDY DESIGN AND SETTING: A survey was mailed to selected practicing ENT physicians, investigating regional information, practice type, IGS usage patterns, perceived benefits and limitations, and usage of the 61795 surgery code. RESULTS: Seventy-three percent of respondents use IGS. Nonusers respond that it provides no benefit or is too expensive. Eighty percent of respondents replied that IGS may allow for increased safety in certain procedures. Most users attempt reimbursement with the 61795 code. CONCLUSION: IGS usage is increasing but appears to be perceived as expensive and nonbeneficial in certain situations. Most respondents, however, felt that IGS may lead to safer surgery in certain situations, including revision and frontal procedures. Several factors appear to limit routine use including ease of use, technical setup, code reimbursement, and initial purchase costs. SIGNIFICANCE: IGS use appears to be increasing. The most frequent users appear to agree with the previously issued AAO-HNS guidelines regarding appropriate indications. Expanded use may depend on ease of use, reimbursement, and affordability. EBM rating: D-5.     

Cocaine abuse, attention deficit disorder, and bipolar disorder

Cocaine is a potent dopamine agonist that frequently stimulates the central nervous system and is often manifested by increased psychomotor activity, impulsivity, euphoria, and rapid thoughts. Attention deficit disorder (ADD) and bipolar disorder also present with physical restlessness, racing thoughts, distractibility, and mood instability. Although these three disorders rarely appear in the same individual, they are important differential diagnoses when considering any one illness with the above symptom complexes. We report two cases of cocaine abuse with ADD residual type in patients who were previously diagnosed as having atypical bipolar disorder. The adverse effects were reversed by the dopamine agonist bromocriptine.     

Safety and efficacy of atorvastatin in heart transplant recipients.

BACKGROUND: Pravastatin and simvastatin prolong survival and reduce transplant-related coronary vasculopathy, although low-density lipoprotein (LDL) lowering with these agents is only modest. The objective of this study was to assess the safety of moderate dose atorvastatin and its efficacy when prior treatment with another statin had failed to lower LDL to < 100 mg/dl. METHODS: Data from 185 patients were retrospectively evaluated for adverse events, duration of exposure (person-days), and the mean atorvastatin dose exposure. Changes in lipid parameters, and prednisone and cyclosporine doses were determined. RESULTS: Safety: 48 patients received atorvastatin for 24,240 person-days at a mean dose exposure of 21 +/- 10 mg. Rhabdomyolysis, myositis, myalgias, and hepatotoxicity occurred in 0, 2, 2, and 0 patients, respectively. All events occurred at the 10-mg dose, within the first 3 months, and were rapidly reversible with atorvastatin discontinuation. Efficacy: Thirty-four patients evaluable for efficacy analyses had a pre-atorvastatin LDL of 145 +/- 38 mg/dl on the following statins: pravastatin (n = 30, 40 +/- 0mg), fluvastatin (n = 3, 33 +/- 12 mg), simvastatin (n = 1, 40 mg). After atorvastatin (21 +/- 9 mg/day) for 133 +/- 67 days, LDL was reduced to 97 +/- 24 mg/dl (relative reduction 31 +/- 20%, p < 0.0001). At the end of the observation period (418 +/- 229 days, atorvastatin final dose 24 +/- 14 mg/day), LDL was further decreased to 88 +/- 23 mg (relative reduction 37 +/- 17%, p < 0.0001). CONCLUSION: Atorvastatin, when used at moderate doses and with close biochemical and clinical monitoring, appears to be safe and is effective in aggressively lowering LDL in heart transplant recipients when treatment with other statins has failed to achieve LDL goals.     

Regulation of neurotransmitter enzyme by quisqualate subtype glutamate receptors in cultured cerebellar and hippocampal neurons

The possible involvement of ionotropic and metabotropic quisqualate (QA) receptors in neuronal plasticity was studied in cultured glutamtergic cerebellar or hippocampal cells in terms of the specific activity of phosphate-activated glutaminase, an enzyme important in the synthesis of the putative neurotransmitter pool of glutamate. When cerebellar of hippocampal neurons were treated with QA, it elevated the specific activity of glutaminase in a dose-dependent manner. The half-maximal effect was obtained at about 0.1 μM, the maximum increase was at about 1 μM, but levels higher than 10 μM QA produced progressive reduction in glutaminase activity. In contrast, QA had little effects on the activities of lactate dehydrogenase and aspartate aminotransferase and the amount of protein, indicating that the increase in glutaminase was relatively specific. The QA-mediated increase in glutaminase was mimicked by the ionotropic QA receptor agonist -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA; EC₅₀, about 0.5 μM), but not by the metabotropic QA receptor agonist trans-(±)-1-aino-cyclopentyl-1,3,dicarboxyalte (t-ACPD; up to 0.5 mM). The specific ionotropic QA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) inhibited QA- and AMPA-mediated increases in glutaminase activity in a dose-dependent manner, whereas other glutamate receptor antagonists, -2-amino-5-phosphonovalerate, γ- -glutamyl aminomethyl sulphonic acid and γ- -glutamyl diethyl ester were ineffective. The elevation of neurotransmitter enzyme was Ca²⁺-dependent. The increase in Ca²⁺ influx essentially through the activation of L-type voltage-operated Ca²⁺ channels, and not the mobilization of internal Ca²⁺ stores, was responsible for these QA receptor-mediated long-term plastic changes in hippocampal and cerebellar neurons.     

Insulin dependent diabetes in children

We present our experience with twenty children with insulin dependent diabetes mellitus admitted during the past 2 1/2 years. Sixteen patients were admited with acute onset of ketoacidosis while four were having gradual onset. Active and symptomatic treatment was started in all diabetic ketoacidotic patients. One patient died during the acute stage. Eleven patients were followed for 3–6 months or more. Glycosylated hemoglobin was considered as a criteria for control. Three had good control, two fair and six poor control; six developed diabetic ketoacidosis and three developed hypoglycemia