Postherpetic neuralgia

Published on 07/02/2015 by admin

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Last modified 22/04/2025

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Postherpetic neuralgia

Salim Michel Ghazi, MD

The syndrome of postherpetic neuralgia (PHN) is defined as the onset of persistent chronic pain following an attack of acute herpes zoster (AHZ). AHZ is itself a reactivation of the varicella virus that had been dormant following an episode of chickenpox, which usually occurred during childhood.

The pain of AHZ typically subsides within 3 weeks. Whenever the pain of AHZ lasts for more than 4 to 6 weeks, a diagnosis of PHN is suspected. Although PHN has been defined in different ways, recent data support making a distinction among acute herpetic neuralgia (within 30 days of rash onset), subacute herpetic neuralgia (30-120 days after rash onset), and PHN (defined as pain lasting at least 120 days from rash onset).

Overall, pain persists in a chronic form in 10% to 15% of patients following AHZ infection. This incidence is higher if the following well-established risk factors are present: older age, greater severity of acute pain during AHZ infection, more severe rash, a prodrome of dermatomal pain before onset of the rash, cancer, diabetes, immunosuppression, and lymphoproliferative disorders. Patients with these risk factors may have as much as a 50% to 75% risk of having pain that persists for at least 6 months after rash onset. PHN is more common after ophthalmic herpes than after the spinal segment type.

Description of the syndrome

The persistence of pain—described as continuous, burning, and lancinating—that spreads along a single dermatome from the central dorsal line in a ventral direction following the initial rash of AHZ is the most typical manifestation of the syndrome of PHN. The pain is unilateral, most commonly affecting a thoracic dermatome or the ophthalmic division V₁ of the trigeminal nerve (cranial nerve V). Lumbar, cervical, and sacral involvement is less common. Occasionally, but rarely, the pain of PHN can occur without a preceding rash.

In PHN, the affected area typically shows changes in the form of pigmentation and scarring where the vesicles of AHZ have healed. Hyperesthesia, hyperpathia, and allodynia may be present. The pain can often be excruciating and intractable, impairing quality of life to the point that the patient may contemplate suicide. The pain of PHN is purely neuropathic.

Pathophysiology

After the initial infection of herpes zoster, usually many years previously, the virus remains dormant in the dorsal root ganglion of the peripheral nerve. The cause of its reactivation is not fully understood but could be related to a perturbation in the immune system, an increase in stress, or both. The reactivation causes the findings seen in AHZ. The dermatomal distribution of the vesicular rash seen in AHZ is related to the transport of the reactivated virus along the sensory nerve fiber to the skin.

Pathologic changes in AHZ and PHN are characterized by inflammatory changes, followed by necrosis and then scarring of the dorsal root ganglion, leading to degeneration and destruction of the emerging sensory and motor fibers. The inflammatory processes can also involve the anterior and posterior horns of the spinal cord.

Despite the descriptive pathologic changes noted in AHZ and PHN, the exact mechanism of how pain is generated is unclear. Both peripheral and central mechanisms may be involved.

The peripheral mechanism can be explained by the preferential loss of large-caliber neurons found in PHN. According to the gate control theory of pain, decreased activity of large-fiber neurons may allow increased rates of pain impulses to reach the dorsal horn of the spinal cord.

The central mechanism involves a very complex, anatomic, synaptic reorganization in the dorsal horn caused by increased chronic afferent painful input to the cord and ending in a hyperexcitable state in which nonpainful stimuli are now perceived as pain (wind-up phenomenon).

Treatment

Because of the complex nature of the pathology of PHN, no definitive treatment is available. For this reason, prevention of the PHN is vital and consists of recommendations that individuals older than 60 years of age be vaccinated and, when recurrence is diagnosed, that the AHZ episode be treated early with appropriate antiviral medication and steroids.

Since the pain is purely neuropathic, multiple modalities of therapy have been recommended. They are divided into pharmacotherapy, nerve blocks, and surgical intervention. A balanced combination of modalities has the best potential to achieve the goal of decreasing pain to a level that allows patients a better functional status and improves their quality of life (Table 216-1). Referral to a pain rehabilitation center is recommended when the disease is debilitating to the patient and when the patient’s functional status, emotional status, and quality of life are severely impaired.

Table 216-1

Treatment Options for Postherpetic Neuralgia

Pharmacotherapy	Nerve Blocks	Surgical Interventions
Gabapentin Pregabalin Amitriptyline NSAIDs Tramadol EMLA cream Lidoderm cream and patch Opioids Capsaicin cream and patch	Epidural local anesthetic injection Intrathecal steroid injection Lumbar sympathetic block Pulsed radiofrequency denervation of DRG Radiofrequency denervation of intercostal nerves SCS Subcutaneous nerve stimulation	DREZ Motor cortex stimulation Nucleotractotomy

EMLA, Eutectic mixture of local anesthetics; DREZ, dorsal root entry zone lesioning; DRG, dorsal root ganglion; NSAIDs, nonsteroidal antiinflammatory drugs; SCS, spinal cord stimulation.

Because transcutaneous electrical nerve stimulation has minimal side effects and typically provides at least moderate results, these units should also be tried along with pharmacotherapy.

Pharmacotherapy

Pharmacotherapy should include an initial trial of the antiepileptic agent gabapentin, starting at a low dose and gradually increasing the dose to reach 1800 to 2400 mg/day, unless improvement or major adverse effects occur. If the patient does not tolerate gabapentin, pregabalin can be tried to a maximum dose of 300 to 600 mg/day. Tricyclic antidepressant medications can also be used if no results were obtained with gabapentin or pregabalin or adverse effects were not tolerated. Amitriptyline (25-50 mg initial dose at night), nortriptyline, trazodone, and doxepin have been used with variable success. Other medications used with variable success include nonsteroidal antiinflammatory drugs; tramadol; various topical creams, including capsaicin and EMLA cream (eutectic mixture of local anesthetics); and a lidocaine patch. Recently, a patch containing high concentration of capsaicin (8%) was made available in the United States.

Opioid medications can be used and have been found to be helpful in well-selected patients. The use of opioid medications for patients with chronic long-term nonmalignant pain should follow strict rules, with the patient being well informed on the proper use of the medication and establishing treatment goals in association with the health care provider, understanding the risks and consequences of nonadherence to well-detailed instructions. Methadone, long-acting morphine, and long-acting oxycodone have been used for the treatment of PHN, with short-acting medications provided for breakthrough pain. The medication dose should be titrated to effectiveness. If or when patients develop tolerance, they should be switched to another opioid medication. Patients who are receiving opioid medications for the treatment of PHN should be informed that, if they show any sign of abuse, they will be switched to a different treatment.

Nerve blocks

Central, spinal, and sympathetic nerve blocks have shown good but variable results in the treatment of PHN. One study indicated that lumbar sympathetic blocks provided up to 90% improvement in pain score up to 29 months. Intrathecal injection of steroids may be effective, but this treatment is still controversial. Another technique that has been used with some success is the epidural injection of a local anesthetic agent with steroids during the first 2 months of an AHZ infection. More randomized controlled trials are needed to reach a better understanding of the true efficacy of these procedures.

Emerging interventions for the treatment of PHN have been numerous in the last few years and include pulsed or routine radiofrequency denervation of the intercostal nerve roots/dorsal root ganglion, implanted spinal cord stimulators, and implanted subcutaneous peripheral nerve stimulation (not to be confused with transcutaneous nerve stimulation). Of all of these interventions, spinal cord stimulation looks most promising in controlling the pain of PHN over the long term and in improving quality of life.

Surgical procedures

Surgical interventions for the treatment of PHN include dorsal root entry zone lesioning, spinal trigeminal nucleotractotomy, and stereotactic radiosurgery of the trigeminal root. These procedures should be used only when all other modalities have failed.

Nicolas Chamfort, an eighteenth century French writer, said, “Philosophy, like medicine, has plenty of drugs, few good remedies, and hardly any specific cure.”

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