Assessment of cerebral function during cardiopulmonary bypass.
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Biomedical subjects
Publications and source records attributed to L M Kitahata.
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Pain has been a major concern of humankind since the ancient times, and it remains one of the most important subjects of all health care professionals. Despite the obvious overwhelming clinical importance, the major advances in its diagnosis and therapy have been made only recently. "How do the sensory apparatus of the body and system of signal transmission relate to pain of peripheral origin?" is the topic of discussion. To do this, it is important to understand what constitutes the total pain experience. It consists of: 1) signal transduction at the peripheral receptor site, 2) signal conduction along the peripheral nerve, 3) pain modulation at the level of the spinal cord, 4) pain perception at the supraspinal site, and 5) the associated sensations, emotional reactions, and effective state. The signal transmission related to pain may be modified by various analgesic agents. Specific analgesic agent has a specific site of action which may be at peripheral receptors, at peripheral nerves, at the level of the spinal cord, at supraspinal levels by activating descending inhibitory systems, or at more cephalad levels by reducing the affective component of pain.
BACKGROUND AND OBJECTIVES: The present study examined whether sphenopalatine ganglion block (SPGB) causes a reduction in the response to acute nociceptive input that may account for the SPGB-induced relief reported by many patients with chronic pain. METHODS: In a double-blind, crossover design, 16 healthy volunteers underwent separate 15-minute submaximal effort tourniquet tests before and after SPGB with 20% lidocaine plus 1:100,000 epinephrine (SPGBlidocaine) or placebo (SPGBsaline). Responses during each minute of tourniquet inflation were converted to a 1 to 16 scale and classified as nothing (1), mild sensation (2-4), strong sensation (5-7), slightly painful (8-10), definitely painful (11-13), and severely painful (14-16). RESULTS: Maximum pain scores reached 12.6 +/- 2.5 (mean +/- SD) pre-SPGB, 10.9 +/- 3.5 after SPGBsaline, and 11.1 +/- 2.5 after SPGBlidocaine. No significant differences were noted between SPGBlidocaine and SPGBsaline at any of the 15 time points (p = NS by repeated measures ANOVA and paired t-test). However, retrospective grouping of time points noted that scores after SPGBlidocaine were lower in the "strong sensation" range. CONCLUSION: SPGB does not lessen acute extremity pain to a significant degree and is not in and of itself an effective means of analgesia for acute pain. Its potential impact on nociceptive stimuli that elicit a "strong sensation" (i.e., a score of 5-7 in the present study) should be evaluated in hyperpathic pain states and in states with exaggerated aversive responses.