Narihito Iwashita

Results of Intradiscal Pulsed Radiofrequency for Lumbar Discogenic Pain: Comparison with Intradiscal Electrothermal Therapy

Background We have developed an intradiscal pulsed radiofrequency (Disc PRF) technique, using Diskit II® needles (NeuroTherm, Wilmington, MA, USA), as a minimally invasive treatment option for chronic discogenic low back pain (LBP). The purpose of this study was to compare the representative outcomes of Disc PRF and Intradiscal Electrothermal Therapy (IDET) in terms of pain relief and reduction of disability. Methods Thirty-one patients with chronic discogenic LBP who underwent either Disc PRF (n = 15) or IDET (n = 16) were enrolled in the study. A Diskit II® needle (15-cm length, 20-gauge needle with a 20-mm active tip) was placed centrally in the disc. PRF was applied for 15 min at a setting of 5 × 50 ms/s and 60 V. The pain intensity score on a 0-10 numeric rating scale (NRS) and the Roland-Morris Disability Questionnaire (RMDQ) were assessed pretreatment and at 1, 3, and 6 months post-treatment. Results The mean NRS was significantly improved from 7.2 ± 0.6 pretreatment to 2.5 ± 0.9 in the Disc PRF group, and from 7.5 ± 1.0 to 1.7 ± 1.5 in the IDET group, at the 6-month follow-up. The mean RMDQ also showed significant improvement in both the Disc PRF group and the IDET group at the 6-month follow-up. There were no significant differences in the pretreatment NRS and RMDQ scores between the groups. Conclusions Disc PRF appears to be an alternative to IDET as a safe, minimally invasive treatment option for patients with chronic discogenic LBP.

Proton magnetic resonance spectroscopy assessment of metabolite status of the anterior cingulate cortex in chronic pain patients and healthy controls

Background Chronic pain is a common cause of reduced quality of life. Recent studies suggest that chronic pain patients have a different brain neurometabolic status to healthy people. Proton magnetic resonance spectroscopy (1H-MRS) can determine the concentrations of metabolites in a specific region of the brain without being invasive. Patients and methods We recruited 56 chronic pain patients and 60 healthy controls to compare brain metabolic characteristics. The concentrations of glutamic acid (Glu), myo-inositol (Ins), N-acetylaspartate (NAA), Glu + glutamine (Glx), and creatine + phosphocreatine (total creatine [tCr]) in the anterior cingulate cortex of participants were measured using 1H-MRS. We used age- and gender-adjusted general linear models and receiver-operating characteristic analyses for this investigation. Patients were also assessed using the Hospital Anxiety and Depression Scale (HADS) to reveal the existence of any mental health issues. Results Our analysis indicates that pain patients have statistically significantly higher levels of Glu/tCr (p=0.039) and Glx/tCr (p<0.001) and lower levels of NAA/tCr than controls, although this did not reach statistical significance (p=0.052). Receiver-operating characteristic analysis performed on the combination of Glx/tCr, Ins/tCr, and NAA/tCr effectively discriminated chronic pain patients from healthy controls. Patients with higher HADS-Depression scores had increased Glx/rCr levels (p=0.015), and those with higher HADS-Anxiety scores had increased NAA/tCr levels (p=0.018). Conclusion Chronic pain patients have a different metabolite status in the anterior cingulate cortex to controls. Within the pain patient group, HADS scores had a positive relationship with NAA/tCr and Glx/tCr levels. 1H-MRS successfully detected metabolic changes in patients’ brains in a noninvasive manner, revealing its potential as a superior diagnostic tool for pain patients.

Involvement of Peripheral NMDA Receptor in Melittin-Induced Thermographic Flare

Intradermal injection of an active compound of European honeybee toxin, melittin, into the forearm in humans produces temporary pain and evokes sustained increase of local skin temperature. This increase of skin temperature is suppressed by the pretreatment of a voltage gated sodium channel blocker, lidocaine, suggesting that neurogenic inflammation is involved in the skin temperature increase after the melittin treatment. In this study, we tested a hypothesis that the melittin-induced skin temperature increase is augmented by an N-methyl-D-aspartate (NMDA) glutamate receptor that is present on the peripheral terminals of cutaneous primary afferents. Skin temperature was examined after the local application of incremental doses of melittin by a computer-assisted-thermography in pentobarbital-anesthetized rats. Local subcutaneous glutamate was collected through a microdialysis probe and glutamate levels were measured by a high pressure liquid chromatography with electrochemical detection method. Intraplantar injection of melittin resulted in the increase of subcutaneous glutamate levels and the increase of local skin temperature, which was partially attenuated by co-injection of an NMDA receptor antagonist, MK-801. In addition, intraplantar injection of NMDA itself increased the local skin temperature. Our data suggest that melittin-induced increase of skin temperature is enhanced through the activation of peripheral NMDA receptors by locally released glutamate. We suggest that topical administration of NMDA receptor antagonists could be an effective treatment of neuro-inflammatory pain.