Published on 07/02/2015 by admin
Filed under Anesthesiology
Last modified 07/02/2015
This article have been viewed 974 times
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.
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.
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.
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