The transient receptor potential ankyrin 1 (TRPA1) channel has been proposed to be a molecular transducer of cold and inflammatory nociceptive signals. It is expressed on a subset of small primary afferent neurons both in the peripheral terminals, where it serves as a sensor, and on the central nerve endings in the dorsal horn. The substantia gelatinosa (SG) of the spinal cord is a key site for integration of noxious inputs. The SG neurons are morphologically and functionally heterogeneous and the precise synaptic circuits of the SG are poorly understood. We examined how activation of TRPA1 channels affects synaptic transmission onto SG neurons using in vitro and in vivo whole–cell patch–clamp recordings in adult rat spinal cord. We have shown that cinnamaldehyde (CA; selective TRPA1 agonist) elicited a barrage of excitatory postsynaptic currents (EPSCs) in a subset of the SG neurons. However, the role of TRPA1 on synaptic transmission in the spinal dorsal horn is not fully understood. In this study, an action of CA was investigated on dorsal root–evoked synaptic transmission to SG neurons in adult rat spinal cord slices by use of the whole–cell voltage–clamp technique. In about 30% of neurons examined, superfusing CA depressed C–fiber–evoked EPSCs. On the contrary, Aδ–fiber–evoked EPSCs were unaffected by CA in all of cells tested. Such a blockade action was not observed when CA was applied in the presence of a specific TRPA1 antagonist, HC–030031. Next, we examined the effects of mechanical stimuli to the skin during TRPA1 activation in the spinal dorsal horn by using in vivo patch clamp technique. Superfusing CA significantly inhibited pinch evoked EPSCs of the skin.

It is concluded that TRPA1 agonist CA specifically acts on a part of C–afferents, resulting in an inhibition of evoked excitatory transmission to the SG; this may contribute to, at least in part, an acute analgesic action of CA such as TRPV1 agonist capsaicin. These findings suggest that activation of spinal TRPA1 channels may have therapeutic potential for the treatment of pain.

Chronic pain is a complex state that involves unpleasant emotion, autono­mic responses, helplessness against pain and movement disorder, as well as the sensation of pain itself. These memorized responses influence the present experience and behavior of the patient. A single treatment option is not enough to treat such a complex clinical state. Thus, our facility has several treatment programs to fit individual patients’ needs. We applied an individualized hypnotic approach to 161 patients who had not shown satisfactory improvement and were considered suitable subjects for psychotherapy.

A hypnosis session consisted of the introduction stage, which prepared the therapeutic contexts accommodated to the change in chronic pain as well as each patient’s history, and the induction stage, which mainly targeted non–pain body sensations. Among the patients who tried hypnosis, 71.1% experienced in–session analgesia (ISA), and 46.3% experienced out–of–session analgesia (OSA). The most of the first ISA was experienced before approximately the 10^th session, and the most of the first OSA was experienced by approximate­ly the 15th session after ISA.

Based on the process and degree of analgesia, the number of sessions, the leaning rate of self–hypnosis, and the patients’ characteristics and experiences in the above process, we attempted to determine the conditions under which the patients were successfully engaged in hypnosis, the stage of changes in their chronic pain, and the inhibitory factors against analgesia. Despite clinical differences among the patients and their pain situations, their responses to the hypnosis implied the importance of achieving pain cessation through their own therapeutic efforts.

Sixty–five patients (45 male, 20 female; mean age: 71.7 ± 0.9) who under­went microendoscopic muscle preserving interlaminar decompression for lumbar spinal stenosis (LSS) were classified according to degenerative spondylolisthesis and pattern of neurological disorder. We estimated concerning clinical results and association between low back pain (LBP) and lumbar lordosis (LL). Postoperatively, leg symptom as well as LBP significantly improved in all groups. The improvement of LBP was significantly correlated with the increase of LL. Lumbar decompression for LSS may improve LBP and the lumbar alignment regardless of spondylolisthesis and pattern of neurological disorder.

Background: Brain–derived neurotrophic factor (BDNF) may play an important neuromodulatory role in spinal cord. The aim of this study was assessed a relationship between pain–related behavior, expression of BDNF and p38 induced by nucleus pulposus (NP) applied to nerve roots in rats.

Methods: Adult female Sprague–Dawley rats were used. NP was applied to the left L5 DRG of rats in the NP group. In the sham group, the same procedure was performed without NP application on the DRG. The mechanic­al withdrawal threshold was investigated using von Frey hairs. And immunohistochemical analyses of phosphorylated p38 (p38) and BDNF in the spinal cord were observed to colocalize with neuron (NeuN) and microglia (OX42). The numbers of p38 and BDNF immune–reactive (IR) cells in the dorsal horn were counted.

Results: The mechanical withdrawal threshold in the NP group was significant­ly decreased for 35 days compared with that in the sham group. Both p38 and BDNF positive cells were localized with microglia and neurons in spinal cord. In the NP group, the expression of p38–IR and BDNF–IR cells increased from day 2 to 21 compared with the sham group.

Conclusions: According to the results of this study, the mechanical threshold was reduced from 2 days after surgery, and BDNF and p38 were expressed in both activated microglia and neurons in spinal cord. BDNF and p38 expression might be the important role to induce neuropathic pain.