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DOI: 10.1016/J.JHSB.2005.04.010
Herpes Zoster in the Ulnar Nerve DistributionFrom the Hand and Upper Limb Centre, University of Western Ontario, London, Ontario, Canada and Hand Service, Hospital for Special Surgery, New York, USA Correspondence: Dr Andrew J. Weiland, Professor of Surgery, Weill Medical College of Cornell University, Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021, USA. Tel.: +212 606 1575; Fax: +212 535 0426. E-mail: weilanda{at}hss.edu
Varicella zoster is a ubiquitous virus which usually affects school-aged children as Chicken Pox. While the initial disease is self-limiting and seldom severe, the virus remains in the body. It lies dormant in the dorsal root ganglia and reactivation may occur years later with variable presentations as Herpes Zoster, or Shingles. While Shingles is common, it rarely presents exclusively in the upper extremity. It is important that hand surgeons recognize the possibility of zoster infection, with or without a rash, when evaluating the onset of neuralgia in a dermatomal distribution in the upper limb. Early diagnosis allows rapid and appropriate treatment, with a lower risk of complications. We report on a case of Herpes Zoster isolated to the ulnar nerve distribution in a young woman.
Key Words: Herpes Zoster • rash • shingles • peripheral nerve • hand
Varicella zoster virus belongs to the herpes family and is a double-stranded DNA virus which causes two distinct syndromes. The primary infection (Chicken Pox) presents as a highly contagious rash, consisting of clusters of vesicles on the skin and mucous membranes. Subsequent reactivation of latent varicella zoster virus in the dorsal root ganglia or cranial nerves results in a dermatomal cutaneous eruption, Herpes Zoster or Shingles. Symptoms of primary Varicella infection usually resolve within a few weeks. Complications are rare, with the most common being scarring due to excoriation of lesions. The virus is known to remain dormant throughout the affected individual’s lifetime. Although the exact mechanism has not been delineated, the postmortem discovery of viral particles in the dorsal root ganglia and cranial nerves of patients suggests anti-dromic migration to these sites after primary infection. The dormant virus has the ever-present potential for future reactivation, although the mechanism of reactivation is unknown (Gilden et al., 2000). Reactivation, known as Herpes Zoster or Shingles, occurs primarily in older individuals, aged 60–70 years (Merchut and Gruener, 1996; Rosenfeld and Price, 1985). The most common cause of reactivation is the normal age-related decline in cell-mediated immunity (Cohen et al., 1999). Patients with immunosuppressive diseases or on immunosuppressive medications are also more susceptible (Matondo et al., 2000). The annual incidence of Herpes Zoster is about 1.5 to 3.5 cases per 1000 persons (Donahue et al., 1995; Johnson and Dworkin, 2003), and the lifetime risk is estimated to be 10 to 20% (Ragozzino et al., 1982). The prodrome of Herpes Zoster consists of tingling, itching and pain in the involved nerve distribution. The acute phase of the disease consists of variable episodes of fatigue, malaise, and low-grade fever, with intermittent nausea and abdominal pain (Heller and Kelly, 1980). Within a few days an erythematous maculopapular rash erupts, which progresses to clusters of clear vesicles. The vesicles ulcerate and crust and, eventually, heal with possible scarring and pigment changes. Excessive sweating may occur, owing to a process similar to that of reflex sympathetic dystrophy (Lee et al., 1999). Although weakness may be present at the onset of symptoms, it is usually masked by the more prevalent complaint of severe pain (Merchut and Gruener, 1996). The most concerning immediate complication is bacterial super-infection of open vesicles. Long-term complications include post-herpetic neuralgia, cranial nerve symptoms, hepatitis and pneumonitis (Gilden et al., 2000). Shingles can occur in any dermatomal distribution, although it is most common on the trunk. There is a paucity of literature on upper extremity Herpes Zoster and most reported cases involve the radial nerve (Chester, 1992; Nee and Lunn, 1989; Matondo et al., 2000). To our knowledge, there is only a single report of ulnar nerve zoster reactivation in the literature (Matondo et al., 2000), with no reports present in the hand literature. We report on a case of isolated ulnar nerve zoster reactivation in a young woman.
A 36 year-old, right-handed, female administrative assistant presented with a 6 day history of pain along the ulnar aspect of her right distal forearm and wrist. There was no history of trauma or other bone and/or joint involvement. Initially, as the pain progressed, the patient consulted a homeopathic practitioner who diagnosed a soft tissue injury and prescribed a removable forearm-based splint and homeopathic medications. On presentation, the patient was experiencing escalating ulnar wrist pain, parasthesiae in the ulnar nerve distribution and emerging motor weakness of the right hand. Her past medical history was not significant, other than childhood chicken pox. She had no known drug allergies and was taking only multivitamins and silica, as prescribed by her homeopathic practitioner. Examination revealed clusters of erythematous vesicles in the ulnar nerve distribution (Figs 1 and 2). There was decreased light-touch sensation to the ring and little fingers. However, objective two-point discrimination was not measured. There was slight clawing of the ring and little fingers with associated grade 4 intrinsic muscle weakness, according to the Medical Research Council grading system. There was no evidence of Horner’s syndrome, cranial nerve involvement or any other motor weakness.
The patient’s presentation was consistent with Herpes Zoster. Because she presented after 72 hours from vesicular eruption and had few risk factors, antivirals were not prescribed. The patient was referred for medical evaluation and she made an uneventful recovery within three and a half weeks of presentation. She was asymptomatic at 4 month follow-up, with no residual pain, paraesthesiae or weakness. There was no scarring from her vesicular eruption.
The differential diagnosis for localized linear cutaneous eruptions includes lichen striatus, linear psoriasis, inflammatory verrucous epidermal nevus and acute linear eczema (Roholt et al., 1995). Although the characteristic clustered vesicular rash is the most common indicator of zoster reactivation, shingles may occur sine herpete, without any cutaneous manifestations. This presents a diagnostic challenge and such patients may recover without ever having had an accurate diagnosis made. In patients with neoplasia and immunocompromized states, e.g. HIV positive status or on immunosuppressive drugs, the cutaneous lesions may be atypical and require laboratory confirmation. Viral culture, direct immunofluorescence and polymerase-chain reaction assays are available for detecting Varicella zoster (Bezold et al., 2001; Dahl et al., 1997). In patients with motor weakness, electro-diagnostic studies may be helpful to localize lesions. There are several serious complications of Herpes Zoster, including encephalitis, myelitis, neuritis and acute retinal necrosis. However, the most common and feared is post-herpetic neuralgia. Post-herpetic neuralgia is defined as pain that persists for greater that 1 month after the onset of rash (Kost and Straus, 1995). The risk factors for developing post-herpetic neuralgia are increased age, greater acute pain during the rash phase, more severe rash and a prodrome of dermatomal pain before rash onset (Johnson and Dworkin, 2003). Most patients have acute pain associated with shingles and 10–70% go on to develop post-herpetic neuralgia (Kost and Straus, 1996; Ragozzino et al., 1982). Post-herpetic neuralgia may also develop after a pain-free interval (Kost and Straus, 1996). Acyclovir, valacyclovir, famciclovir and brivudin are the four antiviral drugs approved for use in Europe for the treatment of Herpes Zoster, whereas in the United States only three drugs are in use (acyclovir, valacyclovir and famciclovir) (Gross et al., 2003; Scott et al., 2003). These agents inhibit the replication of the Varicella zoster virus, resulting in decreased viral shedding, accelerated healing of lesions and decreased duration and severity of acute pain (Gnann and Whitley, 2002; Johnson and Dworkin, 2003). Antiviral treatment should be initiated in patients with post-herpetic neuralgia risk factors, immunosuppression and zoster ophthalamus (Donahue et al., 1995; Gnann and Whitley, 2002). Ideally, antiviral therapy should be initiated within 72 hours of rash onset (Gilden et al., 2000). However, some patients will still benefit from delayed treatment (Wood et al., 1998). Affected patients should also be aware that they may transmit the virus to others and they should avoid close contact with individuals who are not immunized against varicella. Shingles is uncommon in the upper extremity. However, it is important to include this disease in the differential diagnosis of segmental pain and weakness. In the majority of cases, zoster can be diagnosed on the basis of a thorough history and physical exam, but a rash is occasionally absent, making diagnosis less obvious.
Received for publication December 30, 2004. Accepted for publication April 12, 2005.
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