During the last decade, the neuromatrix theory proposed by Melzack has attracted considerable attention as a basis for exploring the mechanism underlying phantom limb pain. In the neuromatrix theory, emphasis is placed on the role of sensory input as well as motor output in synthesizing the neurosignature that gives rise to the quality of the self, the feeling that all parts of the body are uniquely one's own. This view resembles that of Husserlian phenomenology, which analyzes the formation of body image through changes in sensory experience induced by body movement, termed Kinesthese. The present paper analyzes various clinical findings in patients with phantom limb pain, who were treated by thalamic relay nucleus stimulation, from a phenomenological standpoint, and discusses how the results of such an analysis are reconciled with the neuromatrix theory. While attention has been paid mainly to disturbances of sensory input in investigating the mechanism of phantom limb pain, more research on the role of disturbances of motor output may be needed in order to clarify the exact picture of the pathophysiology of phantom limb pain and to establish an efficient therapeutic approach to this form of pain.

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   Spinal mechanisms of hyperalgesia is believed to be caused by a series of actions, including activation of NMDA receptors with an increase in intracellular NO in the second-order neurons of the spinal cord dorsal horn, activation of guanyl cyclase (GC) and the subsequent activation of protein kinase, and gene expression. We investigated the influence of NO increase on NMDA receptors and the subsequent involvement of GC. Exposed rabbit spinal cords were irrigated with SNP, as an NO source, and WDR neuron activity was measured electrophysiologically by an extracellular microelectrode. Spontaneous and pinching-induced activities of the WDR neurons were also measured after irrigating with SNP only, a mixture of SNP and MK801 (NMDA recep tor antagonist), a mixture of SNP and MB (GC inhibitor), or a mixture of SNP and HB (NO scavenger).
   In the SNP group the numbers of both spontaneous and pinching-induced activities increased, and the increase in neuronal activity after pinching lasted for approximately 2 hours. There were no significant differ ences in the number of either spontaneous or induced activities after administrating the mixture of SNP and MK801 compared to the SNP group.However, the duration of increased activity decreased significantly. In the SNP/MB and SNP/HB groups there was a significant reduction in both spontaneous and induced activities compared to the SNP group.
   From the data above hyperalgesia caused by SNP could be related to NO. Because there was no significant difference in neuronal activity between the SNP group and the mixture of SNP and MK801 group, MK801 seemed not to inhibit hyperalgesia easily once it was induced in the spinal cord dorsal horn. GC activation and cGMP hyperfunction associated with increased NO were assumed to participate in hyperalgesia, as the mixture of SNP and MB did not make significant changes in both spontaneous and induced activities.Both spontaneous and induced activities were stayed in the control level after irrigation with SNP and HB, which confirmed that NO played a role in increasing WDR neuron activity.
   NO delivered from SNP was speculated to continuously increase spontaneous WDR neuron activity, and to accentuate stimuli-induced activity, contributing to central sensitization in the spinal cord.

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   Purpose: Continuous epidural analgesia is increasingly used to manage acute and chronic pain. Epidural analgesia affords profound pain relief, and, in certain high-risk patients, may decrease morbidity, mortality, and treatment costs. However, some investigators have reported that this form of treatment has resulted in the development of epidural abscesses.
   Some investigators have described the antimicrobial properties of local anesthetic agents that have been used in continuous epidural analgesia. It has been suggested that the use of these agents may significantly alter the microbial population.
   The purpose of this study was to determine the risk of growth of Staphylococcus epidermidis in local anesthetics commonly used in clinical practice, specifically 0.5%, 1%, and 2% lidocaine; 0.125%, 0.25%, and 0.5% bupivacaine; and 0.5%, 1%, and 2% mepivacaine.
   Methods: Diluted bacterial suspension of Staphylococcus epidermidis was added to the 0.9% sterile non­bacteriostatic saline or the different local anesthetics. After the organisms were added, a sample from each vial was put into one plate of trypicase soy agar at 0, 0.5, 2 and 4 h intervals for a total of three plates per solution per sampling period. All were stored and incubated at 37˚C in an atmosphere of 5% CO₂ for 24 h. Each plate medium was read and the number of colony-forming units (CFUs) was counted and recorded by the same investigator.
   Results: The number of CFUs declined in proportion to time incubated in all three anesthetics, indicating that all the local anesthetics inhibited the growth of Staphylococcus epidermidis, with the antimicrobial activity of bupivacaine being strongest, followed by lidocaine and then mepivacaine. Effects were proportional to concentration and time: higher concentrations and longer times led to a reduced number of CFUs.
   Conclusions: We conclude that lidocaine, mepivacaine and bupivacaine all inhibit the growth of Staphylo­coccus epidermidis.

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   Background: Trigeminal neuropathy following dental treatment is one of the most difficult conditions to treat. Prolonged abnormal sensation tends to be observed in cases whose nerves were moderately or severely damaged. We previously reported that the severity of nerve injury could be measured with electric and tactile detection thresholds. The purpose of this study was to investigate if stellate ganglion block (SGB) started immediately after nerve injury could be an effective treatment procedure.
   Methods: The present study included 64 damaged and 15 intact trigeminal divisions in 59 patients. Electric detection threshold (EDT) one week after the injury was measured and all divisions were estimated to have an equivalent severity of damage. Damaged nerves were divided into three groups. 1) Nerves followed up without SGB (NSGB: n=17). 2) Nerves that were treated with SGB within two weeks of injury were classified ESGB (n=28), and 3) those with treatment commencing later than two weeks were LSGB (n=19). EDT and type of abnormal sensation (hypoesthesia, allodynia, hyperalgesia and dysesthesia) were periodically recorded throughout twelve months from the injury. EDT in 15 contralateral divisions was repeatedly measured to assure its reproducibility.
   Results: Recovery from hypoesthesia was significantly better in ESGB than other two groups and better in LSGB than NSGB. Furthermore, other types of abnormal sensation on twelve months following injury were less frequently in ESGB.
   Conclusions: These results suggest that early SGB prevented aggravation of the pathology and accelerated recovery of nerve function.

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