Post-Herpetic Neuralgia
Primary varicella infection (chickenpox) is typically a mild and self-limited childhood illness presenting with a characteristic rash (pox), fever, malaise, and fatigue. Following primary infection, the varicella zoster virus (VZV) exists in a clinically
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Daniel Pak and Joseph C. Hung
Introduction
Risk Factors
Primary varicella infection (chickenpox) is typically a mild and self-limited childhood illness presenting with a characteristic rash (pox), fever, malaise, and fatigue. Following primary infection, the varicella zoster virus (VZV) exists in a clinically inactive state in the dorsal root ganglia spinal nerves or sensory ganglia of cranial nerves. The virus can remain latent for years, but has the potential to reactivate as acute herpes zoster (AHZ)—typically seen as a blistering skin rash in the distribution of the affected ganglia. Symptoms are usually self-limited and resolve within several weeks. However, a subset of patients may have persistent pain that can last for months to years. If persistent, this neuropathic pain condition is known as post-herpetic neuralgia (PHN) and is the most common complication from AHZ. Though a 3-month time period for continued pain is typically used as a defining criterion for PHN, time frames in the literature range between 1 and 6 months.
The risk of AHZ increases with advanced age. In the general population, the lifetime risk of AHZ is 25% and escalates to greater than 50% in those older than 80 years. In general, immunocompromised patients are at increased risk for AHZ. Specific examples include advanced age (older than 50), patients with HIV, diabetes, respiratory diseases, and/or cancer, and patients that take medications (e.g., steroids, chemotherapy) that weaken the immune system. There are several risk factors cited in the literature that increase the chance of developing PHN after AHZ. Like AHZ, the elderly are susceptible—nearly 75% of PHN cases are seen in those 60 years and older. Other named risk factors include: female gender, pain/neurologic symptoms prior to rash (prodrome), uncontrolled acute pain, and rash severity during AHZ.
D. Pak, MD Department of Anesthesiology, New York Presbyterian Hospital - Weill Cornell Medical Center, 525 East 68th Street, Box 124, New York, NY 10065, USA
The pain associated with acute herpetic neuralgia is likely due to inflammation and damage to the nerve structures during AHZ. Neural damage is amplified through peripheral and central sensitization mechanisms. Even innocuous afferent input may result in increased spontaneous activity of primary nociceptive and their associated second-order neurons.
J.C. Hung, MD (*) Department of Anesthesiology and Critical Care Medicine, 1275 York Avenue, New York, 10065 e-mail: [email protected]
Pathophysiology
© Springer International Publishing Switzerland 2017 R.J. Yong et al. (eds.), Pain Medicine, DOI 10.1007/978-3-319-43133-8_148
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D. Pak and J.C. Hung
554 Table 148.1 Post-herpetic neuralgia treatment modalities Tricyclic antidepressants (TCA)
Anticonvulsants
Topical Agents
Opioids
Infusion therapies
Cutaneous/electrical nerve stimulation (TENS) Interventional pain techniques
Neurosurgical techniques
Common agents/modalities • Amitriptyline • Nortriptyline • Desipramine • Gabapentin • Pregabalin • Valproic
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