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Background: In this prospective, randomized, double-blind, controlled study, we investigated the sensory, motor and analgesic block characteristics of S(+) ketamine, fentanyl and saline given intrathecally (IT) in addition to 0.5% plain bupivacaine (10 mg) for spinal analgesia. Methods: Ninety ASA I or II adult patients undergoing Caesarean section were randomly allocated to receive 1.0 mL of 0.9% saline in Group S (n = 30), 0.05 mg kg-1 of S(+) ketamine (1.0 mL) in Group K (n=30) or 25 μg (1.0 mL) of fentanyl in Group F (n=30) following 10 mg of plain bupivacaine 0.5% IT. We recorded onset and duration of sensory and motor block, time to reach the maximal dermatomal level of sensory block and duration of spinal analgesia. Results: The onset time of sensory and motor block was significantly shorter in Groups K and F than in Group S (P < 0.014). Their duration was significantly longer in Group F than in Groups K and S (P < 0.009). The time to reach the maximal dermatomal level of sensory block was significantly shorter in Groups K and F than in Group S (P < 0.001). The duration of spinal analgesia was significantly longer in Group F than in Groups K and S (P < 0.001). Conclusion: In patients undergoing Caesarean section with spinal analgesia, the addition of S(+) ketamine (0.05 mg kg -1) IT to 10 mg of spinal plain bupivacaine (0.5%) led to rapid onset of both sensory and motor blockade and enhanced the segmental spread of spinal block without prolonging the duration of spinal analgesia, whereas fentanyl provided prolonged analgesia [ABSTRACT FROM AUTHOR]

Objective: It is unclear to what extent muscle phosphorylase b kinase (PHK) deficiency is associated with exercise-related symptoms and impaired muscle metabolism, because 1) only four patients have been characterized at the molecular level, 2) reported symptoms have been nonspecific, and 3) lactate responses to ischemic handgrip exercise have been normal., Methods: We studied a 50-year-old man with X-linked PHK deficiency using ischemic forearm and cycle ergometry exercise tests to define the derangement of muscle metabolism. We compared our findings with those in patients with McArdle disease and in healthy subjects., Results: Sequencing of PHKA1 showed a novel pathogenic mutation (c.831G>A) in exon 7. There was a normal increase of plasma lactate during forearm ischemic exercise, but lactate did not change during dynamic, submaximal exercise in contrast to the fourfold increase in healthy subjects. Constant workload elicited a second wind in all patients with McArdle disease, but not in the patient with PHK deficiency. IV glucose administration appeared to improve exercise tolerance in the patient with PHK deficiency, but not to the same extent as in the patients with McArdle disease. Lipolysis was higher in the patient with PHK deficiency than in controls., Conclusion: These findings demonstrate that X-linked PHK deficiency causes a mild metabolic myopathy with blunted muscle glycogen breakdown and impaired lactate production during dynamic exercise, which impairs oxidative capacity only marginally. The different response of lactate to submaximal and maximal exercise is likely related to differential activation mechanisms for myophosphorylase.