Intracranial recording during hypnotic analgesia.
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Biomedical subjects
Publications and source records attributed to D E Becker.
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OBJECTIVE: To identify low-frequency activity in the pain-evoked potential at very late latencies, consistent with C-fiber transmission velocities. METHODS: Brief (1 ms) painful (intracutaneous) and two levels of non-painful (mild and strong) electrical pulses were applied to the index and middle fingers of the left hand. Evoked potentials (EPs) were recorded from 30 electrodes covering the entire scalp. Data from the 3 stimulus conditions (approximately 60 trials per condition per subject) were compared using the frequency domain technique of complex demodulation applied to single trial data. Subjects were 14 normal right-handed male human volunteers, aged 19-36 years. RESULTS: Using descriptive probability mapping, pain versus strong non-pain differences were found in grand average data as well as in 8 of 14 subjects, consisting of greater low-frequency power at latencies from 700 to 1100 ms at electrodes near the contralateral central sulcus and at the vertex. CONCLUSIONS: There are topographically focal, pain versus non-pain differences in the 700-1100 ms latency range that can be seen using frequency-domain analytic techniques. These differences were not seen with traditional time domain analyses. They may be due to a C-fiber-related mechanism or to very late activity triggered by faster fibers.
Although laser retinal surgery is the best available treatment for choridal neovascularization, the current procedure has a low success rate (50%). Challenges, such as motion-compensated beam steering, ensuring complete coverage and minimizing incidental photodamage, can be overcome with improved instrumentation. This paper presents core image processing algorithms for 1) rapid identification of branching and crossover points of the retinal vasculature; 2) automatic montaging of video retinal angiograms; 3) real-time location determination and tracking using a combination of feature-tagged point-matching and dynamic-pixel templates. These algorithms tradeoff conflicting needs for accuracy, robustness to image variations (due to movements and the difficulty of providing steady illumination) and noise, and operational speed in the context of available hardware. The algorithm for locating vasculature landmarks performed robustly at a speed of 16-30 video image frames/s depending upon the field on a Silicon Graphics workstation. The montaging algorithm performed at a speed of 1.6-4 s for merging 5-12 frames. The tracking algorithm was validated by manually locating six landmark points on an image sequence with 180 frames, demonstrating a mean-squared error of 1.35 pixels. It successfully detected and rejected instances when the image dimmed, faded, lost contrast, or lost focus.
This paper presents a landmark based method for efficient, robust, and automated computational synthesis of high-resolution, two-dimensional (2-D) or three-dimensional (3-D) wide-area images of a specimen from a series of overlapping partial views. The synthesized image is the set union of the areas or volumes covered by the partial views, and is called the "montage." This technique is used not only to produce gray-level montages, but also to montage the results of automated image analysis, such as 3-D cell segmentation and counting, so as to generate large representations that are equivalent to processing the large wide-area image at high resolution. The method is based on computing a concise set of feature-tagged landmarks in each partial view, and establishing correspondences between the landmarks using a combinatorial point matching algorithm. This algorithm yields a spatial transformation linking the partial views that can be used to create the montage. Such processing can be a first step towards high-resolution large-scale quantitative tissue studies. A detailed example using 3-D laser-scanning confocal microscope images of acriflavine-stained hippocampal sections of rat brain is presented to illustrate the method.
Pain is a protective mechanism for the body; it occurs whenever any tissues are being damaged, and it causes the individual to react to remove the pain stimulus. Most ailments of the body cause pain, and the ability to diagnose different diseases depends to a considerable extent on the physician's knowledge of the various qualities of pain. In dentistry, pain may be expected, i.e., caused by dental procedures, and its management should commence preoperatively. This article is a review of pharmacologic pain management in adult dental patients. It discusses the pharmacology and therapeutic utilization of opioid and nonopioid analgesics and the selection of single and combined analgesic regimens.
Allergic and pseudoallergic reactions can be associated with all drug classes used in dental practice. A thorough medical history is essential to avoid challenging a patient with an agent for which they have proven intolerance. Despite this precaution, the dentist must be prepared to manage an immediate reaction, should it occur. In all cases, management should begin with standard ABC assessment and oxygen supplementation. The administration of either diphenhydramine or epinephrine is predicated on the severity of the reaction. Suggestions regarding dosages and routes of administration are summarized in Table 4. The duration of action for epinephrine is relatively brief (10 to 30 minutes), and dosages may need to be repeated if symptoms recur. Following stabilization, patients who have experienced anaphylactoid reactions should be transported by EMS to the closest emergency room for definitive management. A treatment algorithm summarizing management of allergic reactions is presented in Figure 1.
To help define essential interactions of cGMP with the catalytic site, we tested a series of cGMP analogs as competitive inhibitors of each cyclic nucleotide phosphodiesterase (PDE) family known to hydrolyze cGMP (PDE1, PDE2, PDE3, PDE5, and PDE6). IC50 values, relative to cGMP, were used to predict which functional groups of cGMP contribute to binding by the catalytic sites of each isozyme. The results indicate that the N1-nitrogen of cGMP contributes to binding at the catalytic site of all PDEs, probably as a hydrogen donor. All PDEs tested, with the exception of PDE2, also use the 6-oxo group, probably as a hydrogen acceptor. In contrast to other cGMP-binding enzymes, the 2-amino and 2'-hydroxyl groups of cGMP are not major requirements for binding to any PDE. The 8-bromo- and 8-p-chlorophenylthio-substituted analogs inhibit PDE1, PDE2, and PDE6 activity with high relative affinities, suggesting that these PDEs are not sterically hindered with bulky 8-position substitutions and that they do not preferentially bind the anti-conformation of cGMP. PDE3 and PDE5 have reduced apparent affinity for these analogs and therefore either are sterically hindered with these substitutions or bind cGMP in the anti-conformation. Overall, the data show substantial differences in structural requirements for cGMP binding to the catalytic sites of the different PDE families. Comparisons with published data show different structural requirements for binding to the catalytic, compared with noncatalytic, binding domains of PDEs. Even larger differences are seen between the requirements for binding to PDE catalytic sites and those for the cGMP-dependent protein kinase and the cGMP-gated cation channel.
To define essential interactions of cAMP with the catalytic sites of cyclic nucleotide phosphodiesterases (PDEs) and to begin to map the topology of the sites, we have tested a series of cAMP analogs as competitive inhibitors of the PDEs that hydrolyze cAMP with high efficiency (PDE1, PDE2, PDE3, and PDE4). Comparisons of IC50 values, relative to cAMP, were used to predict which functional groups on cAMP interact with each isozyme. Common to all PDEs tested, except for the calcium/calmodulin-dependent PDE (CaM-PDE, PDE1), is an interaction at the N1-position of cAMP and a distinct lack of binding to the 2'-hydroxyl group of the ribose moiety. Only the cGMP-stimulated (PDE2) and cAMP-specific (PDE4) PDEs appear to interact strongly at the N7-position. The cGMP-inhibited PDE (cGI-PDE, PDE3) may interact less strongly with this nitrogen. The PDE4 and PDE3 both interact with cAMP through the 6-amino group, which most likely serves as a hydrogen bond donor. PDE4 and PDE3 appear to be able to bind to the anti-conformer of cAMP, whereas the PDE1 and PDE2 bind the syn-conformer. The CaM-PDE exhibits no appreciable specificity for any of the analogs tested, showing little or no interaction with the 6-amino group or with any of the ring nitrogens. Large differences exist in the nucleotide-binding requirements for the PDE catalytic sites, compared with the regulatory sites of cAMP-dependent protein kinase and the catabolite activator protein.
The potential for drug interactions is a concern to all dentists. The issue is made even more imposing by the amount of scientific information published each month. It is not only important for dentists to be aware of interactions that have been established, but also those that are no longer tenable. Of particular concern are continued misconceptions about the antibiotic-oral contraceptive and the vasopressor-antidepressant interactions. This article will clarify these issues as well as highlight established interactions associated with those drug classes used most frequently in dental practices.
Drugs that influence autonomic function are used more frequently than surgeons generally imagine. This article summarizes principles of autonomic pharmacology and highlights specific drugs that are useful to the practicing oral and maxillofacial surgeon.
Preoperative assessment and continuous support of respiratory function are essential components of medical care during dental treatment. This article describes the principles of respiratory support and reviews the pathophysiology and management of common disorders that may present acute complications during daily dental practice.
This review article illustrates that all medications used for conscious sedation can depress ventilation. The dental practitioner should not abandon the use of these agents to control fear and anxiety during dental treatment; rather, the dentist should administer the agents cautiously and monitor respiratory status throughout the dental procedure. In this regard, pulse oximetry is a welcomed advance in monitoring as it acts to warn the unknowing clinician that he is approaching a "cliff" (the steep portion of the oxyhemoglobin curve).
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Most incidences of nausea and vomiting can be avoided by careful movement of the patient from a supine position to walking, sound hemostatic principles, and prudent postoperative medication prescribing habits. However, when therapeutic intervention becomes necessary, the clinician should ascertain the probable source of vomiting center activation before selecting a particular pharmacological agent. Although many agents are available, there is little evidence of superior efficacy for agents other than those listed in Table 3.
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