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Postherpetic neuralgia is a chronic pain syndrome that is often difficult to treat and can lead to a disabling disease if it is resistant to therapy. Presented here is the case of a 46-year-old patient with human immunodeficiency virus infection and chronic, treatment-resistant neuralgia. Postherpetic pain resolved after treatment with 1 cycle of subcutaneous recombinant interleukin-2.
Postherpetic neuralgia is defined as pain persisting, or recurring, at the site of shingles at least three months after the onset of the acute rash. Thus defined, at least half of shingles sufferers over the age of 65 years develop postherpetic neuralgia. In addition to increasing age, less important risk factors for postherpetic neuralgia are pain severity of acute shingles and trigeminal distribution. Postherpetic neuralgia accounts for 11-15% of all referrals to pain clinics and would, in fact, be far more effectively dealt with in primary care. Effective treatment of acute shingles by systemic antivirals at the appropriate time may have some effect in reducing the incidence of postherpetic neuralgia, making it easier to treat with tricyclics and greatly reducing scarring (25% of all cases affect the face). Pre-emptive treatment with low-dose tricyclics (ami- or nor-triptyline 10-25 mg nocte) from the time of diagnosis of acute shingles reduces the incidence of postherpetic neuralgia by about 50%. Established postherpetic neuralgia should be vigorously treated with adrenergically active tricyclics in a dose rising over two or three weeks from 10-25 mg to 50-75 mg. Positive relaxation should also be used. Carbamazepine, like conventional analgesics, is of little or no value. Failure of tricyclics to effect relief within eight weeks calls for specialist treatment. North American practitioners in particular believe that some opioids (e.g., oxycodone) may be helpful in otherwise intractable cases.
Postherpetic neuralgia is a disorder that occurs frequently in the elderly. As the effect of the treatment of postherpetic neuralgia is often disappointing, studies have focussed on the prevention of this complaint. A commonly used preventive intervention is the administration ofa single epidural injection of a local anaesthetic and a corticosteroid, combined with oral antiviral agents and analgesics. In a large, multicentre, randomised controlled trial, the investigators found that the single injection of a corticosteroid and a local anaesthetic had no added value in the prevention of long-term postherpetic neuralgia.
Postherpetic neuralgia, which occurs most typically in older persons, is one of the most common and serious complications of herpes zoster (or shingles). It is a chronic neuropathic pain syndrome and remains one of the most difficult pain disorders to treat. Known beneficial agents include antidepressants, antiepileptic drugs, opioid analgesics, local anaesthetics, capsaicin and other, less applied, modalities. Although monotherapy is commonly applied, no single best treatment for postherpetic neuralgia has been identified; nevertheless, gabapentin (antiepileptic) and transdermal lidocaine (anaesthetic) are often used as the first-choice treatments. Recent research has shed light on possible pain mechanisms as well as new avenues of treatment, which are discussed in the article. For patients with pain that is not adequately controlled, individualised treatment plans must be pursued. It is critical to recognise that postherpetic neuralgia, while difficult to manage, can be a treatable neuropathic pain syndrome.
Postherpetic neuralgia was studied in a general-practice population (3,600-3,800) for 26 years, 1947-1972. Postherpetic neuralgia followed 46 (14.3 per cent) of the 321 cases of zoster. No neuralgia occurred after zoster in those under 30 years old. The incidence was strongly associated with age, the highest, 34.4 per cent of the zosters, being in people over 80 years old.Women, especially between 50 and 69 years old, suffered more zoster than men, and women with zoster suffered more postherpetic neuralgia.The incidence of neuralgia was not affected by the anatomical location of the zoster. The duration of neuralgia was unrelated to the age of the patient. Cranial neuralgias lasted much longer on average than neuralgia in other sites. Lumbar and sacral neuralgia were short-lived.
Postherpetic neuralgia (PHN) remains one of the most troublesome common chronic neuropathic pain conditions. Many controlled trials have been published showing good efficacy and reasonable tolerability. These include gabapentinoids, opioids, tricyclic antidepressants, and topical lidocaine and capsaicin. Combination therapies are possible, but have not been proven, and long-term follow-up is limited. Only few case series exist for surgical and other invasive therapies and their role remains uncertain.
Postherpetic neuralgia (PHN) is a persistent neuropathic pain condition after herpes zoster that frequently coexists with sleep disturbance, medication-related problems, and fluctuating symptoms. This study evaluated whether a standardized nursing-led protocol could improve multidimensional short-term outcomes beyond usual care. In this prospective, parallel-group randomized controlled trial, 128 adults with PHN were allocated 1:1 to usual care or usual care plus an eight-week protocol integrating structured pain assessment, sleep monitoring, medication-adherence support, and rule-based digital symptom monitoring. The primary outcome was the between-group difference in change in Numeric Rating Scale (NRS) pain score from baseline to Week 8. Secondary outcomes included Pittsburgh Sleep Quality Index (PSQI), MMAS-8 medication adherence, symptom burden, pain-related nocturnal awakenings, breakthrough pain, rescue analgesic use, adverse events, rule-based alerts, and nursing satisfaction. Week-8 data were available for 116 participants (57 usual care; 59 protocol). Mean NRS scores decreased from 7.19 ± 1.08 to 4.82 ± 1.53 in the usual-care group and from 7.28 ± 1.05 to 3.24 ± 1.28 in the protocol group. An NRS reduction of at least 2 points occurred in 49.1% and 76.3% of participants, respectively. The protocol group also showed larger improvements in PSQI, MMAS-8, symptom burden, and nocturnal awakenings, with fewer breakthrough-pain episodes and less rescue-analgesic use. These findings support further evaluation of the standardized nursing-led protocol in preregistered multicenter trials with intention-to-treat analyses and longer follow-up.
Postherpetic neuralgia is one of the most common, but also one of the most difficult conditions to treat. This condition mainly involves trigeminal, intercostal and sciatic nerves and the brachial plexus area. It mostly appears in patients older than 60 years. Although pain is a transient condition, the pain of postherpeutic neuralgia may become intractable, disabling an may decrease the quality of the patient's life. We studied 30 patients affected by ophthalmic postherpetic neuralgia, appearing, some months after fronto-orbital cutaneous eruption. All patients received nicardipine retard, decreasing gradually, 40 mg/day for 2 weeks. The monitoring of pain was performed using the visual analogue score of Scott-Huskissonn. The results show an improvement in 'pain relief'.
Postherpetic neuralgia, when defined as neuropathic pain persisting 1 month or longer after herpes zoster infection, affects about 10% of all patients who have contracted the disease. The incidence of postherpetic neuralgia increases with age; at age 60, about 50% of herpes zoster patients will suffer significant pain, and this proportion grows with subsequent decades. If therapy is carefully chosen and monitored, it is possible to give satisfactory relief, taking pain from severe to mild, to between 60 and 70% of patients. This article will review current treatment and focus on antidepressant drugs, treatments that are contentious and of current interest such as topical agents, and the use of opioids for this type of chronic neuropathic pain.
Postherpetic neuralgia is a perplexing disorder in which pain develops as a result of herpes zoster. It is a common cause of neuropathic pain and may render its effects especially on the elderly and immunocompromised. Once established, postherpetic neuralgia is resistant to most treatment modalities and can lead to much despair. Many therapeutic approaches have been attempted through the years, most with varying results. This review describes clinical manifestations including allodynia, hyperaesthesia and anaesthesia. It also reviews pharmacologic and non-pharmacologic treatment modalities including a review of anaesthetic nerve blocks, neurostimulation, acupuncture and surgical techniques.
Postherpetic neuralgia is an unfortunate aftermath of shingles, and is most likely to develop, and most persistent, in elderly patients. Pain, allodynia, and sensory loss in the affected dermatome are the cardinal manifestations of the disorder. The pathophysiology of postherpetic neuralgia is not well known, but recent observations suggest multiple changes in the afferent pathways at both peripheral and central nervous system levels.
The efficacy of topical aspirin/diethyl ether (ADE) mixture in the treatment of acute herpetic neuralgia and postherpetic neuralgia, suggested in a previous open-label study (De Benedittis et al. 1992), has been evaluated in a double-blind crossover placebo-controlled study as compared with two other NSAID (indomethacin and diclofenac) drug/ether mixtures. The study included 37 patients (15 with acute herpetic neuralgia (AHN) and 22 with postherpetic neuralgia (PHN)). Comparative treatment results showed that only aspirin (but not indomethacin and diclofenac) was significantly superior to placebo, as compared with baseline and duration of pain relief (P < 0.05 and P < 0.01, respectively), in both AHN and PHN groups. Good-to-excellent results were achieved by 87% of AHN patients and by 82% of PHN patients treated with the ADE mixture, with no significant differences between the two groups. On the whole, patients with trigeminal involvement, less severe pain and with dysaesthetic quality of pain yielded best results.
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 microgram/ml. Topical application of 5% lidocaine gel relieves PHN pain by a direct drug action on painful skin.
Postherpetic neuralgia (PHN), the most frequent complication of varicella-zoster virus (VZV) reactivation, is characterized by pain that persists for greater than 1 mo and often for years after zoster rash. To examine whether PHN might be related to reactivation of VZV, blood mononuclear cells of patients with PHN were tested for the presence of VZV DNA and proteins. VZV DNA was detected in the mononuclear cells of one PHN patient. VZV-specific proteins were detected in mononuclear cells of two acute-varicella patients, one acute zoster patient, and six elderly patients with PHN, but these VZV-specific proteins were not detected in three elderly zoster patients without PHN. Furthermore, pulse-chase experiments revealed further processing or degradation of VZV-specific proteins in the mononuclear cells. These findings strongly suggest that persistence, reactivation, and expression of VZV may result in PHN.
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.
Postherpetic neuralgia (PHN) is a separate disease entity that represents a complication of acute herpes zoster. PHN, involving aberrant somatosensory processing in the peripheral and/or central nervous system, is considered to be a chronic neuropathic pain, frequently unresponsive to all treatment modalities. Despite the clinical trial data demonstrating successful pain relief with several drug regimens, the pharmacologic management of neuropathic pain is difficult, particularly in PHN. Response to therapy is generally inhomogeneous. Some patients experience long-term pain control with either topical or oral monotherapy with antidepressants, anticonvulsants, or opioids. Other PHN patients, such as those suffering pain due to central nervous system lesions, are extraordinarily refractory to all measures. This article will review current treatments--tricyclic antidepressants, anticonvulsants, local anesthetics, clonidine, N-methyl-D-aspartate (NMDA)-antagonists, and opioids and focus on mechanism-based pharmacologic interventions. Pharmacologic approaches can be classified into three groups: 1) drugs that act topically in the affected skin area; 2) drugs that act on nerve excitability and conduction in sensory axons; and 3) drugs that act on neural damage related synaptic changes. This last group is the only pain treatment option related to central denervation. To date, the treatment of PHN has relied on the use of tricyclic antidepressants (TCAs), which represent the most comprehensively studied medications for this pain syndrome. Clinical data indicate that TCAs are effective analgesics in approximately 50% of patients; these drugs have been recommended as first-line agents for all neuropathic pain syndromes except trigeminal neuralgia, but are frequently contraindicated or poorly tolerated in elderly patients with PHN. If monotherapy fails, a mechanism- and/or symptom-based multidrug regimen can be used. There is also consistent support for intravenous and topical lidocaine, intravenous ketamine, carbamazepine, and opioids. Gabapentin, a new anticonvulsant, can be considered a first-line oral medication for PHN based on the efficacy and safety results of a recently completed double-blind trial. In addition to positive effects on PHN, sleep, mood, and overall quality of life were significantly improved.
Postherpetic neuralgia (PHN) is a chronic pain syndrome that disproportionately affects the elderly; its incidence is anticipated to increase as the population ages. PHN presents as pain (continuous burning or intense paroxysmal), most often with tactile allodynia, which may be severe and disabling, resulting in poor quality of life and depression. Traditional treatments have included tricyclic antidepressants, anticonvulsants and opioids; however, adverse systemic effects associated with these agents have led to the development of a newer and potentially safer agent, the topical lidocaine patch 5% (Lidoderm), a targeted peripheral analgesic. This article reviews the clinical pharmacology of the lidocaine patch 5% for the treatment of PHN and summarises data from clinical trials of its safety, tolerability and efficacy. The Medline search terms "lidocaine" and "patch" were used to search for English-language articles on the pharmacokinetics of the lidocaine patch 5% and its clinical use for the treatment of PHN. Additional published studies not identified by the database search but performed by the authors or their colleagues were also included in the review. The systemic absorption of lidocaine from the patch was minimal in healthy adults when four patches were applied for up to 24 hours/day, and lidocaine absorption was even lower among PHN patients than healthy adults at the currently recommended dose. Vehicle-controlled and open-label trials found the lidocaine patch 5%, either alone or in combination with other agents, to be effective in the treatment of PHN. Most adverse events were at patch application sites; no clinically significant systemic adverse effects were noted, including when used long term or in an elderly population.In patients with PHN, the lidocaine patch 5% has demonstrated relief of pain and tactile allodynia with a minimal risk of systemic adverse effects or drug-drug interactions. Because of its proven efficacy and safety profile, the lidocaine patch 5% has been recommended as a first-line therapy for the treatment of the neuropathic pain of PHN.
Postherpetic neuralgia (PHN) is the most common and feared complication of herpes zoster. The more severe and painful the initial zoster outbreak, the more likely that PHN will develop, with elderly patients being at greatest risk. There are no proven treatments that have a large impact in reducing the risk of PHN. Tricyclic antidepressants are the mainstay of treatment for established PHN, aided by transcutaneous electrical nerve stimulation, physical therapy techniques, and cautious use of other medications. Topical agents, such as capsaicin, aspirin, and lidocaine, may soon become one of the mainstays of therapy for PHN.