带状疱疹后遗神经痛患者血清IL-6水平与神经损伤的关系

目的探讨白细胞介素-6(IL-6)与神经损伤和疱疹后遗神经痛(PHN)形成的关系。方法用感觉定量分析仪(TSA2001)对25例PHN患者和29例愈后无PHN的带状疱疹患者的疼痛区及对侧镜像区进行感觉定量测定,同时用ELISA法测定患者血清中IL-6水平。结果PHN患者血清IL-6水平为(386.10±167.51)pg/mL,不仅高于愈后无PHN的带状疱疹患者[(254.40±121.18)pg/mL](P<0.005),而且与其疼痛区的感觉缺失程度呈正相关(r=0.735,P<0.0001)。结论高水平的IL-6作为引起神经损伤的一个重要因素,在形成PHN的过程中具有重要作用。     

氨酚氢可酮联合神经阻滞治疗带状疱疹急性期疼痛的疗效观察

目的观察氨酚氢可酮联合神经阻滞治疗带状疱疹急性期疼痛的疗效。方法选择郑州大学第一附属医院就诊的带状疱疹急性期患者61例,按照随机数字表法分为常规治疗+神经阻滞组(对照组)、常规治疗+神经阻滞+氨酚氢可酮组(实验组)。分别记录所有患者治疗前后视觉模拟评分(VAS),睡眠质量评分(AIS),红外热像扫描皮肤温差(△dT),带状疱疹后遗神经痛(PHN)及其他不良反应发生率。结果与治疗前相比,2组患者治疗后各时间点VAS、AIS评分和红外热像扫描皮肤温差均明显降低(P0.05);与对照组相比,实验组患者治疗后3 d、7 d、14 d VAS评分及AIS评分更低(P0.05),且治疗前后△dT明显更大(P0.05)。2组患者PHN及不良反应的发生率相比未见显著性差异(P0.05)。结论常规治疗联合神经阻滞能够有效缓解带状疱疹急性期疼痛,改善睡眠质量,在此基础上联合氨酚氢可酮使疱疹急性期病程缩短,治疗效果更显著。     

带状疱疹和疱疹后神经痛外周血T淋巴细胞亚群计数与细胞因子表达水平的变化

目的研究带状疱疹(HZ)和疱疹后神经痛(PHN)患者外周血T淋巴细胞亚群和细胞因子的变化,及HZ和PHN的免疫学发病机制。方法选择52例临床确诊的HZ患者,采集外周血,应用流式细胞分析仪检测T淋巴细胞亚群相对计数,应用酶联免疫吸附试验(ELISA)检测细胞因子表达。结果恢复期CD8~+T和CD4~+CD45RO~+T细胞较急性期相显著降低,CD4/CD8比值和CD4~+CD45RA~+T细胞较急性期显著增高,而CD3~+T和CD4~+T细胞无显著差异;与轻中度疼痛组相比,重度疼痛组CD3~+T、CD4~+T和CD8~+T细胞差异无显著变化,CD4/CD8比值和CD4~+CD45RA~+T细胞显著减少,CD4~+CD45RO~+T细胞显著增高;HZ患者恢复期IL-4和IL-10表达较急性期相比显著升高,而IL-17和TNF-显著降低;不同程度疼痛组IL-4、IL-10、IL-17和TNF-α表达无显著差异。结论恢复期HZ与急性期相比T淋巴细胞亚群和细胞因子发生了不同程度变化,重度疼痛与轻中度疼痛患者T淋巴细胞亚群分布有差异,为探讨HZ的发病机制提供了免疫学基础。     

S100β和NSE对带状疱疹后神经痛的监测与疗效评估

目的探讨血清S100β及NSE水平变化与带状疱疹后神经痛(PHN)的发生及治疗前后疗效的关联性。方法收集60例急性带状疱疹(HZ)住院患者,以及20例健康自愿者,运用酶联免疫分析法检测2组治疗前后血清S100β及NSE水平;统计带状疱疹后神经痛的发生率;检测并发带状疱疹后神经痛患者治疗前后血清S100β及NSE的水平变化。结果 60例HZ患者中带状疱疹后神经痛的发生率为13.3%;并发PHN的HZ患者治疗后血清S100β及NSE的水平(69.88±2.28,41.13±6.39)较未发生PHN的HZ患者血清S100β及NSE的水平(54.86±8.90,32.61±8.11)高,差异有统计学意义(P0.05);PHN患者发病前血清S100β及NSE水平(107.36±15.09,98.46±18.25)较治疗后(66.18±7.09,45.34±5.02)明显升高,差异有统计学意义(P0.05);S100β及NSE水平变化与PHN治疗疗效SF-MPQ评分存在正向关联性(P0.05)。结论血清S100β及NSE水平变化与带状疱疹后神经痛发生率及治疗前后疗效存在正向关联性,血清S100β及NSE水平监测可应用于对PHN发生的监测及PHN治疗效果的评估。     

神经阻滞加中药内服治疗带状疱疹神经痛疗效观察

带状疱疹（Herpes Zoster）是由水痘带状疱疹病毒引起的急性炎症性皮肤病,因病毒损伤神经常伴有剧烈的神经痛。治疗原则为止痛、消炎、抗病毒、防止局部感染。急性期止痛不佳会增加患者带状疱疹后神经痛的发病率,给病人带来长期的疼痛症状,严重影响患者的生活质量。本研究对神经阻滞加中药内服治疗带状疱疹神经痛的效果进行观察。     

腺苷钴胺联合普瑞巴林治疗带状疱疹后神经痛疗效观察

带状疱疹后神经痛（post herpetic neuralgia ,PHN ）是指带状疱疹发病后遗留的以感觉神经系统损伤为基础的神经病理性疼痛,多表现为持续性烧灼痛或阵发性刺激痛,可累及全身各处并持续数月至数年不等［1］。8％～24％的急性带状疱疹患者会发生PHN ,而在老年患者中PHN发生率可高达50％［2］。P H N的剧烈疼痛给患者生理和心理上带来极大痛苦,严重影响患者生活质量,但尚无理想的治愈方法。本研究采用普瑞巴林联合腺苷钴胺治疗PHN ,疗效显著,现报告如下。     

带状疱疹后遗神经痛的相关危险因素分析

目的：探讨带状疱疹后遗神经痛的相关危险因素。方法选择我院2012‐07—2014‐07诊治的带状疱疹患者213例。按是否出现神经痛分为带状疱疹后神经痛组和带状疱疹后无神经痛组。比较2组性别、年龄、焦虑或抑郁状态、皮疹部位、急性期疼痛程度,对各主要研究因素进行单因素分析,对差异有统计学意义的因素再进行多因素Logistic回归分析。结果单因素分析显示,2组患者年龄≥50岁、女性、有焦虑或抑郁状态、急性期重度疼痛4个因素上,差异有统计学意义（ P＜0.05）;2组皮疹部位比较差异无统计学意义（P＞0.05）。多因素Logistic回归分析显示,年龄≥50岁、女性、急性期重度疼痛进入回归模型（ P＜0.05）。结论年龄≥50岁、女性、急性期重度疼痛为影响带状疱疹后遗神经疼痛的独立危险因素,重视高年龄、女性及急性期重度疼痛患者早期给予抗病毒及抗病理神经痛可有效预防疱疹后神经痛。     

得宝松预防老年带状疱疹后遗神经痛的疗效分析

目的 观察得宝松预防老年带状疱疹后遗神经痛的临床疗效。方法 选择老年带状疱疹病例146例，实验组90例，除常规治疗方法外，于患者入院后3d内加用得宝松肌注lml 1次；对照组56例，采用常规治疗方法治疗：口服阿昔洛韦0．2g，5次／d，用至疱疹消退，消炎痛25rag，维生素B，20rag，3次／d，口服，用至疱疹消退。结果 实验组的止疱时间、疼痛减轻时间、疼痛消失时间均比对照组短。尤其PHN的发生率显著少于对照组。结论 早期应用得宝松可减少老年患者PHN的发生率。     

带状疱疹性脑膜炎的临床观察(附13例临床分析)

目的:研究带状疱疹性脑膜炎(HZ)的发病机理、临床特点及治疗。方法 了解HZ患者的发病史及既往病史,详细观察其临床表现。13例HZ患者全部脑脊液常规、生化检查、脑电图检查及头颅CT描。结果 部分HZ患者早年曾有水痘病毒(VZV)感染病史,肿瘤病史。临床表现中含颜面,躯干多处出现带状疱疹并有疼痛,多颅神经损害及脑膜刺激征。脑脊液压力增高,细胞数及蛋白增高,脑电图含慢波;CT扫描发现脑内多发低密度灶。部分患者治疗后留有多颅神经损害及疱疹后神经痛。结论HZ可能在VZV初次感染后潜伏在感觉神经内,待机体免疫状态改变时二次发病。应详细了解患者的全部病史,观察其临床特点,并根据病人的免疫状态制定正确的治疗方案。     

单纯疱疹病毒、水痘-带状疱疹病毒感染与脑梗死

目的检测单纯疱疹病毒(HSV)、水痘-带状疱疹病毒(VZV)与脑梗死(CI)的发生是否有相关性。方法采用聚合酶链反应(PCR)的方法来检测入选者病毒DNA。结果 HSV在无常见危险因素死组、高危组及对照组存在差异(P0.05),且组间比较结果为无常见危险因素组与对照组有差异;VZV在脑梗死各组中不存在差异(P0.05)。结论 HSV可能为脑梗死发生的存在关联,VZV与脑梗死的发生无明显相关性。     

VZV vasculopathy and postherpetic neuralgia: progress and perspective on antiviral therapy

Two serious complications of varicella-zoster virus (VZV) reactivation are vasculopathy and postherpetic neuralgia (PHN). Clinical-virologic analyses have proven that VZV vasculopathy is caused by chronic active virus infection in cerebral arteries. Conclusive evidence that PHN is caused by persistent or productive VZV infection is less compelling because human ganglia are not accessible during life for pathologic and virologic examination. However, the notion that PHN may reflect a smoldering VZV ganglionitis is supported by 1) the detection of VZV DNA and proteins in peripheral blood mononuclear cells of many patients with PHN; 2) studies of multiple patients with zoster sine herpete, which indicate a productive VZV ganglionitis; and 3) a favorable response of some patients with zoster sine herpete and PHN to antiviral treatment. Few studies have used antiviral therapy to manage PHN with conflicting results. Larger, double-blind studies, which give IV antiviral drug, are needed.     

Somatosensory findings in postherpetic neuralgia.

Somatic sensory perception thresholds (warm, cold, hot pain, touch, pinprick, vibration, two-point discrimination), allodynia and skin temperature were assessed in the affected area of 42 patients with unilateral postherpetic neuralgia (PHN) and 20 patients who had had unilateral shingles not followed by PHN (NoPHN), and in the mirror-image area on the other side. There was no difference between the two groups for age or length of time after the acute herpes zoster infection. The PHN group showed significant changes in all sensory threshold measurements when the affected area was compared with the mirror-image area on the unaffected side, while the NoPHN group exhibited no threshold changes. Mechanical allodynia was present in 87% of the PHN group; half of the 12 patients with ophthalmic PHN showed extension of allodynia to the maxillary distribution. No differences in skin temperature were recorded between affected and unaffected regions in either group. Our findings show a deficit of sensory functions mediated by both large and small primary afferent fibres and also suggest major central involvement in the pathophysiology of the condition. If PHN does not occur following acute herpes zoster, recovery of neural functions appears to be good.     

Varicella zoster virus-induced pain and post-herpetic neuralgia in the human host and in rodent animal models

Pain and post-herpetic neuralgia (PHN) are common and highly distressing complications of herpes zoster that remain a significant public health concern and in need of improved therapies. Zoster results from reactivation of the herpesvirus varicella zoster virus (VZV) from a neuronal latent state established at the primary infection (varicella). PHN occurs in some one fifth to one third of zoster cases with severity, incidence, and duration of pain increasing with rising patient age. While VZV reactivation and the ensuing ganglionic damage trigger the pain response, the mechanisms underlying protracted PHN are not understood, and the lack of an animal model of herpes zoster (reactivation) makes this issue more challenging. A recent preclinical rodent model has developed that opens up the potential to allow the exploration of the underlying mechanisms and treatments for VZV-induced pain. Rats inoculated with live cell-associated human VZV into the hind paw reliably demonstrate thermal hyperalgesia and mechanical allodynia for extended periods and then spontaneously recover. Dorsal root ganglia express a limited VZV gene subset, including the IE62 regulatory protein, and upregulate expression of markers suggesting a neuropathic pain state. The model has been used to investigate treatment modalities and aspects of pain signaling and is under investigation by the authors to delineate VZV genetics involved in the induction of pain. This article compares human zoster-associated pain and PHN to the pain indicators in the rat and poses important questions that, if answered, could be the basis for new treatments.     

Herpes zoster infection and postherpetic neuralgia

Varicella-zoster virus (VZV), the cause of chicken pox, establishes latent infection in sensory ganglia. Reactivation results in zoster (shingles), sometimes complicated by encephalitis (myelitis). Postherpetic neuralgia (PHN) is the major morbidity of zoster. PHN typically increases in frequency with age. The VZV vaccine, which was developed for children, may be effective in enhancing VZV immune reactivity and decreasing zoster in adults. Early antiviral treatment may be effective in decreasing PHN onset. Several other medications may be useful in treating established PHN. A recent report discussed intrathecal steroid use.     

Postherpetic neuralgia

Following chicken pox infection, varicella-zoster virus stays as a latent infection in sensory root ganglia. After many years, the reactivation of this latent virus in sensory ganglia causes "herpes zoster". Herpes zoster (shingles) is an unilateral, dermatomal, localised, painful, vesicular, and contagious skin infection. In elderly and immunocompromised patients, shingles can cause complications such as postherpetic neuralgia (PHN) and direct central nervous system invasion. Early intervention with antiviral treatment, analgesic therapy and antidepressant therapy may reduce the risk of these complications. The treatment of PHN is same as for other neuropathic pain syndromes. The clinical importance of PHN is due to the severity and chronicity of pain which is usually not responsive to many treatments, and quality of life may be adversely affected by PHN.     

The cancer patient with chronic pain due to herpes zoster

Postherpetic neuralgia (PHN) is the most common complication of herpes zoster, and as such has been an area of extensive medical research for the past three decades. The patients at highest risk for PHN include those older than 50 years, those with severe acute cases of zoster, and those with shingles in a trigeminal distribution. As persons with malignancy are at a high risk for developing zoster itself, PHN is a complication that will be faced by many of these patients and their caregivers. This article reviews the available treatments and preventative measures for this debilitating condition.     

Acute herpetic and postherpetic neuralgia: clinical review and current management

The pain of acute herpes zoster (HZ) may be severe, but it is usually transitory. A minority of patients, with the elderly at particular risk, go on to develop persistent, severe, often disabling pain called postherpetic neuralgia. Though the clinical features of these conditions are well known, the pathology of PHN is poorly described and the pathogenesis of the pain in both remains conjectural. During the past 60 years, an extraordinary number of pharmacological, anesthetic, and surgical therapies have been applied in an attempt to ameliorate the symptoms of acute herpes zoster, enhance its healing, prevent its transition to postherpetic neuralgia, and treat the pain of those with this complication. Relatively few treatments have been studied in a controlled manner, and fully reliable, safe, and effective therapeutic approaches for preventing and treating postherpetic neuralgia have not yet been found. This review summarizes current information on the epidemiology, clinical features, and pathology of herpes zoster and postherpetic neuralgia, and critically examines the accumulated experience with the various treatments. Guidelines for management are suggested.     

Topical lidocaine gel relieves postherpetic neuralgia

Postherpetic neuralgia (PHN) following herpes zoster is a common and disabling neuropathic pain syndrome. In a double-blind, three-session study, 5% lidocaine gel or vehicle was applied simultaneously to both the area of pain and to the contralateral mirror-image unaffected skin. In the local session, lidocaine gel was applied to the painful skin area. In the remote session, lidocaine gel was applied to mirror-image skin. In the placebo session, vehicle was applied bilaterally. For cranial PHN, gel was applied without occlusion for 8 hours. For limb or torso PHN, gel was applied under occlusion for 24 hours. The 16 subjects with cranial PHN reported pain relief significantly favoring local drug application at 30 minutes, 2, 4, and 8 hours. The 23 subjects with torso or limb PHN reported significantly lower pain intensity with local drug application at 8 hours and both pain relief and reduced pain intensity at 24 hours. Remote lidocaine application to mirror-image skin was no different from placebo. No systemic adverse effects were reported and blood levels did not exceed 0.6 μg/ml. Topical application of 5% lidocaine gel relieves PHN pain by a direct drug action on painful skin.     

Postherpetic neuralgia: From preclinical models to the clinic

Postherpetic neuralgia (PHN), a common complication of herpes zoster, which results from reactivation of varicella zoster virus, is a challenging neuropathic pain syndrome. The incidence and severity of herpes zoster and PHN increases with immune impairment or age and may become a greater burden both in terms of health economics and individual suffering. A clearer understanding of the underlying mechanisms of this disease and translation of preclinical outcomes to the clinic may lead to more efficacious treatment options. Here we give an overview of recent findings from preclinical models and clinical research on PHN.     

Chronic varicella-zoster virus ganglionitis—a possible cause of postherpetic neuralgia

Postherpetic neuralgia (PHN) is dermatomal distribution pain that persists for months to years after the resolution of herpes zoster rash. The cause of PHN is unknown. Herein, we report clinical, molecular virological, and immunological findings over an 11-year period in an immunocompetent elderly woman with PHN. Initially, blood mononuclear cells (MNCs) contained varicella-zoster virus (VZV) DNA on two consecutive occasions. Random testing after treatment with famciclovir to relieve pain did not detect VZV DNA. However, the patient was reluctant to continue famciclovir indefinitely and voluntarily stopped drug treatment five times. Pain always recurred within 1 week, and blood MNCs contained many, but not all, regions of the VZV genome on all five occasions. Immunological analysis revealed increased cell-mediated immunity to VZV. Chronic VZV ganglionitis-induced PHN best explains the recurrence of VZV DNA in MNCs whenever famciclovir was discontinued; the detection of only some regions of the viral genome in MNCs, compared to the detection of all regions of the VZV genome in latently infected ganglia; the increased cell-mediated immunity to VZV; and a gratifying clinical response to famciclovir. The presence of fragments of VZV DNA in MNCs likely represents partial degradation of viral DNA in MNCs that trafficked through ganglia during productive infection.