Yasuhiro Maehara

Osteoporosis following chronic constriction injury of sciatic nerve in rats

Abstract. Osteopathic changes sometimes occur in patients with complex regional pain syndrome (reflex sympathetic dystrophy and causalgia). We aimed to investigate whether such osteopathic changes occurred in rats with chronic constriction injury (CCI) of the sciatic nerve. A CCI of the sciatic nerve was established in a unilateral hind limb in 39 adult Sprague-Dawley rats, which were killed 1, 2, 3, 5, or 7 weeks after the CCI procedure. Bone mineral content (BMC) and bone mineral density (BMD) in extracted tibial bones were measured using a dual-energy X-ray absorptiometer, and the number of osteoclasts in the metaphyseal regions was counted by the use of tartrate-resistant acid phosphate (TRAP) staining. BMC was significantly decreased, compared with that of the contralateral side, 1 to 7 weeks after CCI, and BMD was decreased 2 to 7 weeks after the procedure in the ipsilateral tibial bones, compared with BMD in the contralateral bones. The number of TRAP-positive multinucleated osteoclasts in the ipsilateral bones was significantly increased at 2, 3, and 5 weeks after the CCI, when compared with the number of these osteoclasts in the contralateral bones. The results of the present study demonstrate that osteopathic changes are associated with chronic constrictive injury of the sciatic nerve.

Comparison of the in vitro caffeine-halothane contracture test with the Ca-induced Ca release rate test in patients suspected of having malignant hyperthermia susceptibility.

AbstractPurpose. We compared the results of the in vitro caffeine-halothane contracture test (CHCT) according to the protocols of the North American Malignant Hyperthermia Group (NAMHG) and the European Malignant Hyperthermia Group (EMHG) with the Ca-induced Ca release (CICR) rate test in the same patients with suspected malignant hyper thermia (MH). Methods. Five normal controls and 16 patients suspected of having MH susceptibility were studied. Muscle biopsies were usually obtained from the musculus vastus lateralis. Diagnostic cutoff points and procedures for CHCT protocols were as described in the original and renewal versions of NAMHG and EMHGs. The CICR rate test was performed according to the protocol reported by Endo et al. Results. All five normal controls and two patients with abortive MH, two with postoperative hyperthermia, and three with high serum creatine kinase levels were normal in the three tests. Three patients with MH reactions and one patient with a history of masseter spasm were classified as MH positive according to NAMHG criteria and MH susceptible and MH equivocal according to EMHG criteria. There were five cases with discordant results between the CHCT and CICR rate tests. Conclusion. We propose that muscle biopsy for diagnosis of MH susceptibility should combine the CHCT with the CICR rate test, which may identify the defective site of Ca release channels.

Clinical Classification and Incidence of Malignant Hyperthermia in Japan

Denborough and Lovell [1] first described malignant hyperthermia (MH) as an inherited syndrome in 1960. At present, it is generally accepted that MH is triggered by many anesthetics. Succinylcholine chloride (SCC) and volatile anesthetics have been especially implicated as important triggering drugs [2,3]. With these triggering drugs, induced hypermetabolism produces tachycardia, increased O2 consumption and CO2 production, premature ventricular contraction, hypotension and hypertension, cyanosis, tachypnea, muscle rigidity, and hyperthermia as the signs of MH. Also seen as complications of MH are electrolyte imbalances, myoglobinuria, hyperkalemia, creatine phosphokinase (CPK) elevation, impaired coagulation, renal failure, and severe metabolic and respiratory acidosis.