Acute Herpes Zoster of the First Division of the Trigeminal Nerve

The Clinical Syndrome

Herpes zoster is an infection disease that is caused by the varicella-zoster virus (VZV), which also is the causative agent of chickenpox (varicella). Primary infection in the nonimmune host manifests itself clinically as the childhood disease chickenpox. It is postulated that during the course of primary infection with VZV, the virus migrates to the dorsal root or cranial ganglia. The virus then remains dormant in the ganglia, producing no clinically evident disease. In some individuals, the virus may reactivate and travel along the sensory pathways of the first division of the trigeminal nerve, producing the pain and skin lesions characteristic of shingles. The reason that reactivation occurs in only some individualsis not fully understood, but it is theorized that a decrease in cell-mediated immunity may play an important role in the evolution of the disease entity by allowing the virus to multiply in the ganglia and spread to the corresponding sensory nerves, producing clinical disease. Patients who are suffering from malignancies (particularly lymphoma), who are receiving immunosuppressive therapy (chemotherapy, steroids, radiation), or who are suffering from chronic diseases are generally debilitated and 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 be the reason for the propensity for shingles to develop. This may also explain why the incidence of shingles increases dramatically in patients older than age 60 and is relatively uncommon in persons younger than age 20.

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 may attack the geniculate ganglion, resulting in hearing loss, vesicles in the ear, and pain. This constellation of symptoms is called the Ramsey-Hunt syndrome and must be distinguished from acute herpes zoster involving the first division of the trigeminal nerve.

The pain of acute herpes zoster of the first division of the trigeminal nerve will often precede onset of the characteristic vesicular rash.

Signs and Symptoms

As viral reactivation occurs, ganglionitis and peripheral neuritis cause pain, which is generally localized to the segmental distribution of the first division of the trigeminal nerve. This pain may be accompanied by flulike symptoms and 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, often leading to erroneous diagnosis. However, in most patients, the clinical diagnosis of shingles is readily made when the characteristic rash appears. Like chickenpox, the rash of herpes zoster appears in crops of macular lesions, which rapidly progresses to papules and then to vesicles. As the disease progresses, the vesicles coalesce and crusting occurs. The area affected by the disease can be extremely painful, and the pain tends to be exacerbated by any movement or contact (e.g., with clothing or sheets). As healing takes place, the crusts fall away, leaving pink scars in the distribution of the rash that gradually become hypopigmented and atrophic.
In most patients, the hyperesthesia and pain generally resolve as the skin lesions heal. In some, however, pain may persist beyond lesion healing. This most common and feared complication of acute herpes zoster is called postherpetic neuralgia, and the elderly are affected at a higher rate than the general population suffering from acute herpes zoster. The symptoms of postherpetic neuralgia can vary from a mild self-limited problem to a debilitating, constantly burning pain that is exacerbated by light touch, movement, anxiety, and/or temperature change. This unremitting pain may be so severe that it can completely devastate the patient’s life, and ultimately it can lead to suicide. It is the desire to avoid this disastrous sequel to a usually benign self-limited disease that dictates the clinician use all possible therapeutic efforts for the patient suffering from acute herpes zoster in the first division of the trigeminal nerve.

Age of patients suffering from acute herpes zoster.

Treatment

The therapeutic challenge of the patient presenting with acute herpes zoster involving the first division of the trigeminal nerve is twofold: (1) the immediate relief of acute pain and symptoms and (2) the prevention of complications, including postherpetic neuralgia. It is the consensus of most pain specialists that the earlier in the natural course of the disease that treatment is initiated, the less likely it is that postherpetic neuralgia will develop in the patient. Furthermore, because the older patient is at highest risk for developing postherpetic neuralgia, early and aggressive treatment of this group of patients is mandatory.

Nerve Blocks

Sympathetic neural blockade with local anesthetic and steroid via stellate ganglion block appears to be the treatment of choice to relieve the symptoms of acute herpes zoster involving the first division of the trigeminal nerve as well as to prevent the occurrence of postherpetic neuralgia. Sympathetic nerve block is thought to achieve these goals by blocking the profound sympathetic stimulation that is a result of the viral inflammation of the nerve and gasserian ganglion. If untreated, the sympathetic hyperactivity can cause ischemia secondary to decreased blood flow of the intraneural capillary bed. If this ischemia is allowed to persist, endoneural edema forms, increasing endoneural pressure and causing a further reduction in endoneural blood flow with irreversible nerve damage.

As vesicular crusting occurs, the addition of steroids to the local anesthetic may decrease neural scarring and further decrease the incidence of postherpetic neuralgia. These sympathetic blocks should be continued aggressively until the patient is pain free and should be reimplemented at the return of pain. Failure to use sympathetic neural blockade immediately aggressively, especially in the elderly, may sentence the patient to a lifetime of suffering from postherpetic neuralgia. Occasionally, some patients suffering from acute herpes zoster involving the first division of the trigeminal nerve may not experience pain relief from stellate ganglion block but will respond to blockade of the trigeminal nerve.

Adjunctive Treatments

The application of ice packs to the lesions of acute herpes zoster may provide relief in some patients. Application of heat will increase pain in most patients, presumably because of increased conduction of small fibers, but is beneficial in an occasional patient and may be worth trying if application of cold is ineffective. Transcutaneous electrical nerve stimulation and vibration may also be effective in a limited number of patients. The favorable risk-to-benefit ratio of these modalities makes them reasonable alternatives for patients who cannot or will not undergo sympathetic neural blockade or tolerate pharmacologic interventions.

Topical application of aluminum sulfate as a tepid soak provides excellent drying of the crusting and weeping lesions of acute herpes zoster, and most patients find these soaks soothing. Zinc oxide ointment may also be used as a protective agent, especially during the healing phase when temperature sensitivity is a problem. Disposable diapers can be used as an absorbent padding to protect healing lesions from contact with clothing and sheets.

Low intensity laser therapy as well as a coordinated wellness program is also effective in treating this disorder.

Low Intensity Laser Therapy (LILT)

The low intensity Laser (LILT) sends photons (light) into the injured tissues and can penetrate two to three inches to treat affected areas. It uses a natural enhancement of the cellular machinery that can and has been dynamically measured in published studies to promote healing without burning affected tissue. Once the photons find the injured tissues, they stimulate and energize the cells to repair and strengthen at a remarkable rate. The treatment does not hurt, takes about 30 minutes and is very cost advantageous.

Wellness Program

A wellness program whichindividualizes treatment for age, performance and function has been shown in pilot studies to improve the overall health and well being of the individuals evaluated. A well conceived dietary and supplementary regimen based on scientific age–related decline in certain necessary compounds can improve quality of life, correct the ravages of hormone imbalance, balance critical neurotransmitter function without resorting to powerful drugs for depression that often have unfavorable side-effect profiles and restore vitality and youth in daily exercise routines. Furthermore, when wellness products are utilized with success, individuals often seek less costly interventions including unnecessary surgeries and narcotic options to treat pain. For more information go to www.drpwellness.com.