Abstract
Herpes zoster is an infectious disease caused by the varicella-zoster virus (VZV). Primary infection with VZV in a nonimmune host manifests clinically as the childhood disease chickenpox. Investigators have postulated that during the course of the primary infection, the virus migrates to the dorsal root of the thoracic nerves, where it remains dormant in the ganglia and produces no clinically evident disease. In some individuals, the virus reactivates and travels along the sensory pathways of the thoracic nerves to produce the pain and skin lesions characteristic of herpes zoster, or shingles. Although the thoracic nerve roots are the most common site for the development of acute herpes zoster, the first division of the trigeminal nerve may also be affected.
Why reactivation occurs in some individuals but not in others is not fully understood. Investigators have theorized, however, that a decrease in cell-mediated immunity may play an important role in the evolution of this disease by allowing the virus to multiply in the ganglia and spread to the corresponding sensory nerves, thus producing clinical disease. Patients who are suffering from malignant (particularly lymphoma) or chronic disease and those receiving immunosuppressive therapy (chemotherapy, steroids, radiation) are generally debilitated and thus are much more likely than the healthy population to develop acute herpes zoster. These patients all have in common a decreased cell-mediated immune response, which may also explain why the incidence of shingles increases dramatically in patients older than 60 years and is relatively uncommon in those younger than 20 years.
Keywords
acute herpes zoster, postherpetic neuralgia, zoster sine herpete, gabapentin, pregabalin, chest wall pain, diabetic trucal neuropathy, thoracic radiculopathy, devil’s grip, Tietze’s syndrome
ICD-10 CODE B02.9
Keywords
acute herpes zoster, postherpetic neuralgia, zoster sine herpete, gabapentin, pregabalin, chest wall pain, diabetic trucal neuropathy, thoracic radiculopathy, devil’s grip, Tietze’s syndrome
ICD-10 CODE B02.9
The Clinical Syndrome
Herpes zoster is an infectious disease caused by the varicella-zoster virus (VZV). Primary infection with VZV in a nonimmune host manifests clinically as the childhood disease chickenpox. Investigators have postulated that during the course of the primary infection, the virus migrates to the dorsal root of the thoracic nerves, where it remains dormant in the ganglia and produces no clinically evident disease. In some individuals, the virus reactivates and travels along the sensory pathways of the thoracic nerves, to produce the pain and skin lesions characteristic of herpes zoster, or shingles. Although the thoracic nerve roots are the most common site for the development of acute herpes zoster, the first division of the trigeminal nerve may also be affected.
Why reactivation occurs in some individuals but not in others is not fully understood. Investigators have theorized, however, that a decrease in cell-mediated immunity may play an important role in the evolution of this disease by allowing the virus to multiply in the ganglia and spread to the corresponding sensory nerves, thus producing clinical disease. Patients who are suffering from malignant (particularly lymphoma) or chronic disease and those receiving immunosuppressive therapy (chemotherapy, steroids, radiation) are generally debilitated and thus are much more likely than the healthy population to develop acute herpes zoster. These patients all have in common a decreased cell-mediated immune response, which may also explain why the incidence of shingles increases dramatically in patients older than 60 years and is relatively uncommon in those younger than 20 years.
Signs and Symptoms
As viral reactivation occurs, ganglionitis and peripheral neuritis cause pain that may be accompanied by flulike symptoms. The pain generally progresses from a dull, aching sensation to dysesthetic or neuritic pain in the distribution of the thoracic nerve roots ( Fig. 69.1 ). In most patients, the pain of acute herpes zoster precedes the eruption of rash by 3 to 7 days, and this delay often leads to an erroneous diagnosis (see “ Differential Diagnosis ”). However, in most patients, the clinical diagnosis of shingles is readily made when the characteristic rash appears. As in chickenpox, the rash of herpes zoster appears in crops of macular lesions, which rapidly progress to papules and then to vesicles ( Fig. 69.2 ). Eventually, the vesicles coalesce, and crusting occurs. The affected area can be extremely painful, and the pain tends to be exacerbated by any movement or contact (e.g., with clothing or sheets). As the lesions heal, the crust falls away, leaving pink scars that gradually become hypopigmented and atrophic.
In most patients, the hyperesthesia and pain resolve as the skin lesions heal. In some patients, however, pain persists beyond lesion healing. This common and feared complication of acute herpes zoster is called postherpetic neuralgia, and older patients are affected at a higher rate than is the general population suffering from acute herpes zoster. The symptoms of postherpetic neuralgia can vary from a mild, self-limited condition to a debilitating, constantly burning pain that is exacerbated by light touch, movement, anxiety, or temperature change. This unremitting pain may be so severe that it completely devastates the patient’s life; ultimately, it can lead to suicide. To avoid this disastrous sequela to a usually benign, self-limited disease, the clinician must use all possible therapeutic efforts in patients with acute herpes zoster of the thoracic nerve roots.
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