OVERHEATING IN BED AS AN IMPORTANT FACTOR IN MANY COMMON DERMATOSES

Background. Extensive questioning of patients with a wide variety of skin disorders led to the impression that nocturnal overheating was probably an important factor in the initiation and the perpetuation of many skin disorders. Methods. In order to test the hypothesis, 12 “clean-skinned” subjects (6M/6F) aged 18 to 45 years were monitored electronically every 30 seconds during an 8 hour sleep period (2300 to 0700 hours), sleeping under a standard 10 tog duvet. Results. All the subjects were too hot by 3 to 4°C. All showed changes in their EEG patterns with reduced REM sleep, increased awakenings, and all showed changes in their sleep stage patterns. In addition, they all showed evidence of increased sweating in the “heat-sink” area. Conclusions. The mechanisms where by such changes could be implicated in the precipitation and perpetuation of skin disease are discussed. “Lifestyle” modification as a very effective, noninvasive, therapeutic regime is recommended. Further research along these lines would probably be very valuable and instructive.     

Titration of Power Output During Radiofrequency Catheter Ablation of Atrioventricular Nodal Reentrant Tachycardia

Radiofrequency lesions in the anterior, superior aspect of the tricuspid annulus result in selective elimination of fast pathway function in patients with typical atrioventricular (AV) nodal reentry tachycardia. This technique is simple and effective, but has been associated with a significant risk of inadvertent complete AV block. The purpose of this study was to compare the safety and effectiveness of two different techniques for radiofrequency catheter ablation of the fast AV nodal pathway. Initially, a fixed power output was used at each target site. This method was compared retrospectively to a newer technique where power output was gradually incremented at each site. Radiofrequency power was initially applied at 10 watts for 10–15 seconds. If no junctional ectopy or a change in PR intervoi was seen, power output was incremented by 2 to 4 watts every 10 to 15 seconds up to a maximum of 30 watts. Thirty seven of 38 (96%) patients treated using this incremental power output were cured of their AV nodal reentry tachycardia. None of these patients developed inadvertent complete AV block. In contrast, 92% of historic controls treated with a fixed power output between 20 and 30 watts achieved a primary success and nine of these 89 (10%) historic controls developed inadvertent complete AV block (P = 0.04). There was no difference in the amplitudes of atrial, His, or ventricular electrograms at the effective sites between the two groups. Conclusions: (1) the anterior approach to radiofrequency catheter ablation of typical AV nodal reentry is associated with a significant risk of inadvertent complete AV block if a fixed power output is used; (2) starting at low power and gradually incrementing the output during radiofrequency energy application reduces the risk of complete AV block; (3) this incremental technique does not compromise efficacy.     

Lack of Delayed Neurotoxic Effect after Tri-o-cresyl Phosphate Treatment in Male Fischer 344 Rats: Biochemical, Neurobehavioral and Neuropathological Studies

Lack of Delayed Neurotoxic Effect after Tri-o-cresyl PhosphateTreatment in Male Fischer 344 Rats: Biochemical, Neurobehavioral,and Neuropathological Studies. SOMKUTI, S. G., TIL-SON, H. A.,BROWN, H. R., CAMPBELL, G. A., LAPADULA, D. M., AND ABOU-DONIA,M. B. (1988). Fundam. Appl. Toxicol. 10, 199-205. Tri-o-cresylphosphate (TOCP), which produces a delayed neurotoxic syndromein humans and some animal species, was given to Fischer 344(F344) male (18 week old) rats to determine if it causes biochemical,sensorimotor, and neuropathological effects. Animals were givenTOCP by gavage in doses ranging from 10 to 100 mg of TOCP/kgdaily for a period of 63 days. The rats were subjected to aseries of neurobehavioral tests including fore- and hindlimbgrip strength, motor activity, tremor, and latency to respondto a thermal stimulus. Central and peripheral nervous tissueswere examined for damage characteristic of organophosphorouscompound-induced delayed neurotoxicity (OPIDN). Brain neurotoxicesterase and acetylcholinesterase activities were inhibitedin a dose-dependent fashion. A group of three chickens treatedwith 100 mg of TOCP/kg/day for 18 days was included as the positivecontrol for enzymatic and histopathological alterations associatedwith OPIDN. Rats showed no consistent neurobehavioral changesor evidence of neuropathological damage in nervous tissues associatedwith treatment. In contrast, chickens treated with TOCP developeddelayed neurotoxicity characterized by ataxia, which progressedto paralysis. These neurological changes included swelling,fragmentation, and degeneration of the axon and myelin in bothcentral and peripheral nervous tissues. This study concludesthat the F344 rat is not sensitive to the delayed neurotoxiceffects of TOCP. When studying OPIDN in rats, care must be exercisedin choosing the experimental animal since some strains, e.g.,F344, are not sensitive.     

Effects of Toluene Inhalation on Carbon Dioxide Production and Locomotor Activity in Mice

Effects of Toluene Inhalation on Carbon Dioxide Production andLocoraotor Activity in Mice. BUSHNELL, P. J., EVANS, H. L.,AND PALMES, E. D. (1985). Fundam. Appl. Toxicol.. 5,971-977.Rapid and noninvasive tests of locomotor activity (LA) and carbondioxide production (minute volume expired CO₂, or _ECO₂)in mice were sensitive to the effects of inhaled toluene. Comparedto sham exposures, toluene at 100 ppm had no effect on LA or_ECO₂; at 1000 and 3000 ppm, LA increasedduring exposure, while _ECO₂ was suppressedfor 6 to 24 min at the beginning of exposure. In a nominal 10,000-ppmexposure, toluene levels were increased from 1000 to 10,500ppm in 60 min. At these levels, toluene abolished LA at concentrationsabove 8000 ppm, and suppressed _ECO₂ throughoutexposure. During recovery from toluene-induced narcosis, bothLA and _ECO₂ were elevated above control.In other studies, groups of mice inhaled toluene daily at 0,100, 1000, or 3000 ppm, 5 hr/day for 8 or 90 days, and weretested individually 30 to 90 min after termination of exposure.Under these conditions, toluene decreased postexposure _ECO₂ for 1–2 weeks, altered the weekly patternof change in _ECO₂, and did not affect LA.No effects of repeated, daily exposure to toluene were observedon body weight. These results demonstrate the utility of thepresent method to detect changes in LA and metabolic rate resultingfrom toluene inhalation, and suggest that different mechanismsare involved in the behavioral and metabolic responses to tolueneinhalation.     

Carbon Dioxide Production by Individual Mice as an Index of Behavioral and Metabolic Activity

Carbon Dioxide Production in Individual Mice as an Index ofBehavioral and Metabolic Activity. BUSHNELL, P. J., EVANS, H.L., AND PALMES, E. D. (1985). Fundam. Appl. Toxicol.. 5,962-970.A noninvasive method for simultaneous real-time determinationof spontaneous locomotor activity (LA) and CO₂ production (asminute volume expired CO₂, or _ECO₂) in miceis described. As an apical measure of overall metabolic activity,_ECO₂ proved sensitive to changes in manyphysiological processes, including behavioral activity. In normalmice, LA (as photobeam breaks) and _ECO₂ werepositively correlated (r = 0.73), and stable over repeated dailytests. Food deprivation for 18 hr overnight increased LA whiledecreasing _ECO₂. Stimulation of peripheralsympathetic activity, either by exposure to cold air or by injectionof epinephrine, increased _ECO₂ without affectingLA. Intoxication with pentobarbital produced a biphasic changein both measures: anesthetic doses increased LA and _ECO₂ during induction and recovery, and reduced themduring the period of anesthesia itself. These results characterize_ECO₂ as an easily quantifiable, compositeindex of behavioral and metabolic activity in mice. This measure,along with its covariation with LA, may provide better informationabout toxic effects than any single screening test.     

The Surgical Treatment of Cervical Œsophageal and Laryngopharyngeal Dysphagia

An account is given of the atiology and treatment of common conditions which cause dysphagia in the laryngopharynx and the cervical ?sophagus. Management of cancer is discussed in some detail. Discussion of foreign body and benign strictures due to corrosives and acid regurgitation has been excluded.