Abstract
The first division of the trigeminal nerve is the second most common site of acute herpes zoster infection, after the thoracic dermatomes. In most patients the pain of acute herpes zoster preceeds the eruption of vesicular rash by three to seven days. The rash has a classic vesicular appearance, making the clinical diagnosis of shingles straightforward in most patients. In some patients, the pain of shingles persists beyond skin lesion healing. This persistent pain is known as postherpetic neuralgia. Treatment of acute herpes zoster involving the trigeminal nerve is aimed at acute pain relief and the prevention of postherpetic neuralgia. The use of stellate ganglion block combined with adjuvant analgesics and adjunctive therapies can usually achieve these goals.
Keywords
acute herpes zoster, trigeminal nerve, ophthalmic division, stellate ganglion block, Ramsay Hunt syndrome
ICD-10 CODE B02.22
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 (varicella). Investigators have postulated that during the course of this primary infection, the virus migrates to the dorsal root or cranial ganglia, where it remains dormant and produces no clinically evident disease. In some individuals, the virus reactivates and travels along the sensory pathways of the first division of the trigeminal nerve, where it produces the characteristic pain and skin lesions of herpes zoster, or shingles.
Why reactivation occurs in some individuals but not in others is not fully understood, but investigators have theorized 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, spread to the corresponding sensory nerves, and produce clinical disease. Patients who are suffering from malignant disease (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.
The first division of the trigeminal nerve is the second most common site for the development of acute herpes zoster, after the thoracic dermatomes. Rarely, the virus attacks the geniculate ganglion and results in hearing loss, vesicles in the ear, and pain ( Fig. 1.1 ). This constellation of symptoms is called Ramsay Hunt syndrome and must be distinguished from acute herpes zoster involving the first division of the trigeminal nerve.
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 first division of the trigeminal nerve. 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 with chickenpox, the rash of herpes zoster appears in crops of macular lesions that rapidly progress to papules and then to vesicles ( Fig. 1.2 ). Eventually, the vesicles coalesce, and crusting occurs ( Fig. 1.3 ). 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 persons are affected at a higher rate than is the general population suffering from acute herpes zoster ( Fig. 1.4 ). 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 trigeminal nerve .
Testing
Although in most instances the diagnosis is easily made on clinical grounds, confirmatory testing is occasionally required. Such testing may be desirable in patients with other skin lesions that confuse the clinical picture, such as in patients with acquired immunodeficiency syndrome who are suffering from Kaposi sarcoma. In such patients, polymerase chain reaction testing and immunofluorescent antibody testing can rapidly identify herpes zoster virus and distinguish it from herpes simplex infections ( Fig. 1.5 ). In uncomplicated cases, the diagnosis of acute herpes zoster may be strengthened by obtaining a Tzanck smear from the base of a fresh vesicle; this smear reveals multinucleated giant cells and eosinophilic inclusions ( Fig. 1.6 ). However, this inexpensive bedside test does not have the ability to distinguish between lesions caused by the varicella-zoster virus and herpes simplex infections.
