オピオイド鎮痛薬の中でも強オピオイドに分類されている医療用麻薬は，周術期，苦痛を伴う検査，がんに直接起因する痛み，急性痛，非がん性慢性疼痛と幅が広く，それぞれの病態に沿って適切に使用する必要がある。そこで本邦のオピオイド鎮痛薬の適正使用推進の一助となるよう国外からの最新の知見を得ることを目的として，第42回日本疼痛学会の招聘講演ではEija Kalso先生に「Chronic pain and opioids —how to control proper prescribing ?」のタイトルでご講演頂いた。今回，Eija Kalso先生のご許可を得て本講演の内容を要訳したので紹介する。

注釈：Kalso先生が本講演でオピオイドやオピオイド鎮痛薬として示されている薬物は，主に本邦において医療用麻薬に分類され強オピオイドとして扱われている薬物となる。本稿では本邦でも普及した呼称をとり入れて，強オピオイドと弱オピオイドの名称の後には鎮痛薬という文字はつけていない。

In this review we introduce the nature of NGF molecule, NGF receptor TrkA, NGF producing cells, role of NGF in differentiating nociceptors, and influences of NGF on axonal properties and terminal branching. NGF is essential for the survival and differentiation of sympathetic neurons and neural crest–originated small DRG neurons to nociceptors in fetal life. Expression of TrkA changes along the day after birth: More than 80% DRG neurons express TrkA in fetus, but this percentage decreases after birth to 45% in 14 days, instead percentage of isolectin B4–binding neurons increases from 0% on birth to 40% in 14 days after birth. TrkA is expressed mainly in small DRG neurons, and percentages of neurons expressing TrkA are different depending on tissues ⁄ organs. Notably larger neurons (possibly innervating proprioceptors) also express TrkA in skeletal muscle innervating DRG neurons, and majority of bone innervating DRG neurons are presumed to express TrkA. NGF influences axonal properties such as maximal frequency to follow, axon potential duration and activity dependent slowing. Altogether NGF has deep influences on nociception.

Acetaminophen is widely used for the treatment of fever and pain. Although the analgesic effect of acetaminophen had been previously thought to be due to its anti–inflam­matory action by inhibiting prostaglandin production based on cyclooxygenase inhibition, it is currently considered that acetaminophen exerts its analgesic effects through the central actions of AM404, a metabolite of acetaminophen. However, the central mechanism is not yet fully understood. In the present study, we focused on the locus coeruleus (LC), which contains the largest population of noradrenergic neurons and is known as one of the descending pain modulatory systems, and investigated whether local administration of AM404 into the LC, or systemic application of acetamino­phen altered LC neuronal firing using an in vivo mouse extracellular rescoring technique. As results, we found that local LC administration of AM404, but not acetamino­phen, increased the firing frequency of LC neurons. Systemic acetaminophen application had also a similar excitatory action on LC neuronal activity. These results suggest that AM404, a metabolite of acetaminophen, acts centrally on the LC to increase its neuronal firing frequency. This central action may be one of the mechanisms for analgesic action of acetaminophen.

Background: Effects of pulse irradiation with a 10–W semiconductor laser on pressure pain threshold and temporal summation were examined.

Methods: The subjects were 10 healthy adults. All subjects were participated in both irradiation and sham groups. The irradiation group, 10–W semiconductor laser were applied to thenar eminence of non–dominant hand. The sham group was sham irradiated. Pressure pain threshold and temporal summation at the laser irradiated site were measured before and after irradiation.

Results: The pressure pain threshold value showed a significant increase after 10–W semiconductor laser irradiation only in the irradiation group, but visual analogue scale value reflecting the temporal summation did not change in the both groups.

Conclusion: We conclude that 10–W semiconductor laser irradiation increased the pressure pain threshold. On the other hand, under the conditions of this study, 10–W semiconductor laser irradiation did not affect the temporal summation.