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In some herpes zoster patients, pain persists for more than 3 months or more after healing of vesicular eruptions; this condition is termed postherpetic neuralgia (PHN). We have recently reported the association of the human histocompatibility leukocyte antigens (HLA) haplotype, HLA-A*3303-B*4403-DRB1*1302 with PHN patients; however, it has not been determined whether the haplotype is also associated with herpes zoster that did not develop subsequent PHN. To distinguish whether the haplotype is associated with herpes zoster or the development of PHN, we examined if herpes zoster patients without subsequently PHN are also associated with the HLA haplotype or not. Herpes zoster patients were followed up for more than 6 months, and HLA alleles and haplotypes were compared among the PHN patients (n = 52) the herpes zoster patients who did not develop PHN (n = 42) and healthy controls (n = 125). The frequencies of the risk haplotype in the PHN patients, in the healthy controls and in the herpes zoster patients without subsequent PHN were 16.3, 5.2 and 4.8%, respectively. While the frequency of the risk haplotype was significantly higher in the PHN patients than in the healthy controls (P = 0.0006) no difference was observed between the herpes zoster patients without subsequent PHN and the healthy controls. No significant association was found between the duration of symptoms or the site of herpes zoster and the HLA alleles and the haplotype. These results suggest that the HLA-A*3303-B*4403-DRB1*1302 haplotype plays an important role in the development of PHN after herpes zoster, but not in the onset of herpes zoster.

Herpes zoster is a common disease caused by reactivation of the varicella zoster virus (VZV). In a small number of herpes zoster patients, pain persists beyond 4 weeks or more after healing of vesicular eruptions; this condition is termed postherpetic neuralgia (PHN). Positive associations of human histocompatibility leukocyte antigens (HLA) class I antigens, A33 and B44, with PHN in the Japanese population have been reported. Our hypothesis is that susceptibility genes to PHN might exist in the HLA region and the study objective is to further examine possible associations of genes in HLA class I, II and III regions, HLA-A, -B, -DRB1, tumor necrosis factor a (TNFA) promoter, and a natural killer cell activating receptor, NKp30 polymorphisms with PHN. Although TNFA or NKp30 in the class III region had been considered as a candidate locus, we found no associations of TNFA promoter or NKp30 polymorphisms with PHN in this study. We demonstrated that HLA-A*3303, -B*4403 and -DRB1*1302 alleles were significantly associated with PHN (P ¼ 0.0007 for A*3303, P ¼ 0.001 for B*4403 and P ¼ 0.001 for DRB1*1302). The frequency of the HLA-A*3303-B*4403-DRB1*1302 haplotype was also significantly higher in the PHN patients than in the healthy controls (P ¼ 0.0039). Our results suggest that this haplotype might be related to the pathogenesis of PHN.

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the lateral site of the right leg as well as the dorsal and plantar sites of the right foot. The patient was initially treated at a dermatology clinic with oral valaciclovir (an antiviral agent) and diclofenac (an anti-inflammatory agent), and subsequently, with diclofenac alone for several weeks. Within a month of its onset, the pain in the leg and the dorsum of the foot subsided concomitantly with the skin rash healing. However, severe pain in the plantar site of the foot persisted.Three months after the initial onset, the patient presented at our pain clinic, in a wheelchair, because of intractable pain with severe tactile allodynia on the sole and on the heel of the right foot, which was so severe that it prevented her from walking normally. Resting spontaneous pain was moderate, being rated at 50 mm/ 100 mm on the visual analog scale (VAS). However, marked tactile allodynia was observed on the right heel, which was rated at 91/100 mm. Because of the severe touch-evoked allodynia, she could not stand on the right foot, nor could she wear a sock or shoe on the right foot. She could hardly walk, limping and relying mostly on the left foot, stepping on the right tiptoe, and she wore beach sandals. She was treated initially with oral amitriptyline and repeated (caudal) epidural blocks, which resulted in only a slight improvement in her pain status.Five months after the onset of pain, she was admitted to our hospital to study the mechanisms underlying her pain condition, and to seek potentially effective therapeutic measures. After obtaining institutional review board approval and written informed consent from the patient, we assessed various intravenous (IV) drugs for analgesic efficacy. Because the severe tactile allodynia was elicited most prominently when she was trying to walk, she was asked to rate her pain using VAS both at rest (for spontaneous pain) and when standing/stepping (for evoked tactile allodynia) before, during, and after administration of each test drug.

This pilot study demonstrated that clinical aromatherapy was clinically safe but did not lead to statistically significant improvements in BPSD or ADL among people with dementia. Further research on therapeutic effects is needed to develop high-quality care with clinical aromatherapy for elderly patients with dementia in Japan and to fully establish evidence for effective and safe practice in health care institutions.

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Intravenous ATP exerted slowly developing and long-lasting analgesic effects in half of patients with PHN. Patients with ketamine-responsive PHN were likely to respond to ATP.