It was in 1960 that the first malignant hyperthermia (MH) was reported as the anesthetic deaths in a family. Since then, such cases have been found all over the world and been shown in high morality rate. As being named as it is, a specific sign of MH is the characteristically rapid rise of body temperature of a patient during general anesthesia. Through a series of study on MH, abnormal function of skeletal muscle was found as the cause. Especially in 1970, the sensitivity for muscle contracture to caffeine was found in a MH patient's muscle. In the study using the skinned fiber technique, Endo pointed out in 1977 that the calcium-induced calcium release (CICR) rate of serceplasmic reticulum is accelerated in the MH patient. In early 1990s, through the genetic study based on porcine stress syndrome, an animal model of MH, ryanodine binding channel was the exact cite of abnormality of MH. One point gene mutation was found corresponding to this ryanodine channel. The amino acid alternation was proposed. Since the channel for CICR is the ryanodine binding channel, the functional abnormality of CICR of MH is confirmed by the corresponding genetic abnormality. In North America and Europe, MH is diagnosed by this high sensitivity for muscle contraction to caffeine and halothane using muscle bundle taken from patients. On the other hand, in Japan, MH is diagnosed based on clinical criteda of MH signs and symptoms. According to the clinical diagnosis, the CICR rate of MH muscle has been examined in Japan. The high specificity for diagnosis of MH was obtained by the CICR test. In order to refine undoubted MH patient, the crucial clinical criteria are set in Japan. Thereby, it is helpful to investigate the cause of MH. The criteria are based on two category of symptoms. One is the body temperature (body temperature indicates 40 C or higher, or rate of temperature rise is 0.5 C / 15 min or more). The other is the clinical signs and symptoms found prior to the rise of body temperature (muscle rigidity, tachycardia, arrhythmia, unstable blood pressure, cyanosis, respiratory and metabolic acidosis, sweating, rapid blue change of soda lime, heating of anesthesia circuit, and so on ) Fluminant MH should be satisfied with the condition of category one, and should show several sings and symptoms of category two. The rest of the cases are classified as abortive MH. The case of early finding and success of treatment can be classified as an abortive MH. Such patients might have been classified as fluminant MH, if they were not found early enough or were not treated early and properly. Mechanism for onset of MH may well be explained as follows. The factors for the acceleration of CICR rate are volatile anesthetic agent and heat (direct action on CICR channel), and succinylcholine (by increased intracellular Ca concentration caused by depolarization of muscle cell). Since the CICR function is accelerated per se in MH patient, triggering factor may induce positive feedback of CICR function, whereas, in normal patient, these factors act as a normal pharmacological and physiological responses. In excessive high concentration of intramuscular Ca concentration might cause sustained muscle contraction and hypermetabolic state. These abnormal responses could exhibit the muscle rigidity which is typical abnormal muscle sign of MH, tachycardia which might result from hypercarbia due to hypermetabolism, and increase of body temperature due to hypermetabolism and so on. The specific therapeutic agent, dantrolene, which works on CICR channel, cuts the positive feedback of CICR function. By the progress of genetic study on MH, it is expected to be diagnosed by the blood sampling.