The management of postherpetic pain and dysesthesia can be a trying matter for both the patient and the physician. It is likely that incomplete interruption of nerve impulses results in a hyperpathic state in which every stimulus excites pain. In a number of controlled studies, amitriptyline proved to be an effective therapeutic measure. Initially, it is given in doses of approximately 50 mg at bedtime; if needed, the dosage can be increased gradually to 125 mg daily. The addition of carbamazepine, gabapentin, pregabalin, valproate or one of the serotonin reuptake inhibitor drugs may further moderate the pain, particularly if it is of lancinating type.
Capsaicin ointment can be applied to painful skin, as noted above. A salve of two aspirin tablets, crushed and mixed with cold cream or chloroform (15 mL) and spread on the painful skin, was reported to be successful in relieving the pain for several hours (King). The effect of nerve root blocks is inconsistent, but this procedure may afford temporary relief. In one randomized trial, the preemptive use of epidural steroids at the onset of the rash had minimal effects (van Wijck et al). It should be emphasized that postherpetic neuralgia eventually subsides even in the most severe and persistent cases but the short-term use of narcotics is appropriate when the pain is severe. Until the pain subsides, the physician must exercise skill and patience and avoid the temptation of subjecting the patient to one of the many surgical measures that have been advocated for this disorder (see Chap. 7 for further discussion of pain management). Some patients with the most persistent complaints, beyond a year, have symptoms of a depressive state and will be helped by antidepressive medications.
Retroviruses are a large group of RNA viruses, so called because they contain the enzyme reverse transcriptase, which permits the reverse flow of genetic information from RNA to DNA. Two families of retroviruses are known to infect humans: (1) the lentiviruses, the most important of which is the HIV, the cause of AIDS, and (2) the oncornaviruses, which include the human T-cell lymphotropic viruses (HTLV-I), the agents that induce chronic T-cell leukemias and lymphomas (HTLV-II) and tropical spastic paraparesis (HTLV-I).
The HIV-Acquired Immunodeficiency
In 1981, physicians became aware of the frequent occurrence of otherwise rare opportunistic infections and neoplasms—notably Pneumocystis carinii pneumonia and Kaposi sarcoma—in otherwise healthy young homosexual men. The study of these patients led to the recognition of a new viral disease caused by HIV, AIDS.
HIV infection is characterized by an acquired and usually profound depression of cell-mediated immunity as manifest by cutaneous anergy, lymphopenia, reversal of the T-helper–to–T-suppressor cell ratio—more accurately, CD4+/CD8+ lymphocytes, the result of reduction in CD4+ cells—and depressed in vitro lymphoproliferative response to various antigens and mitogens. It is this failure of immune function that explains the development of a wide range of opportunistic infections and unusual neoplasms. Moreover, the nervous system is susceptible to a number of unusual syndromes that are the direct result of the HIV infection. Virtually all organ systems are vulnerable, including all parts of the CNS, the peripheral nerves and roots, and muscle. AIDS is currently defined as either a CD4+ below 200 cells/μL due to HIV or the presence of opportunistic infections related to HIV immunodeficiency, as such, representing the most advanced stages of HIV infection.