The Uncommon Localization of Herpes Zoster.

INTRODUCTION: Herpes zoster is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV) that is the cause of varicella. It is an acute neurological disease which can often lead to serious postherpetic neuralgia (PHN). Different nerves can be included with the skin rash in the area of its enervation especially cranial nerves (CV) and intercostal nerves. CASE REPORT: In this report we present a patient with herpes zoster which involved ulnar nerve with skin rash in the region of ulnar innervations in women with no disease previously diagnosed. The failure of her immune system may be explained by great emotional stress and overwork she had been exposed to with neglecting proper nutrition in that period. CONCLUSION: Herpes zoster may involve any nerve with characteristic skin rash in the area of its innervations, and failure in immune system which leads reactivation of VZV may be caused by other factors besides the underlying illness.

Isolated ulnar dorsal cutaneous nerve herpes zoster reactivation.

Herpes zoster is a viral disease presenting with vesicular eruptions that are usually preceded by pain and erythema. Herpes zoster can be seen in any dermatome of the body but most commonly appears in the thoracic region. Herpes zoster virus is typically transmitted from person to person through direct contact. The virus remains dormant in the dorsal ganglion of the affected individual throughout his or her lifetime. Herpes zoster reactivation commonly occurs in elderly people due to normal age-related decline in cell-mediated immunity. Postherpetic neuralgia is the most common complication and is defined as persistent pain or dysesthesia 1 month after resolution of the herpetic rash. This article describes a healthy 51-year-old woman who experienced a burning sensation and shooting pain along the ulnar dorsal cutaneous nerve. Ten days after the onset of pain, she developed cutaneous vesicular eruption and decreased light-touch sensation. Wrist and fourth and fifth finger range of motion were painful and slightly limited. Muscle strength was normal. Nerve conduction studies indicated an ulnar dorsal cutaneous nerve lesion. She was treated with anti-inflammatory and antibiotic drugs and the use of a short-arm resting splint. At 5-month follow-up, she reported no residual pain, numbness, or weakness. Herpes zoster in the upper extremity may be mistaken for entrapment neuropathies and diseases characterized by skin eruptions; ulnar nerve zoster reactivation is rarely seen. The authors report an uncommon ulnar dorsal cutaneous nerve herpes zoster reactivation. Clinicians should be aware of this virus during patients' initial evaluation.

Herpes zoster in the ulnar nerve distribution.

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.

Sabin attenuated LSc/2ab strain of poliovirus spreads to the spinal cord from a peripheral nerve in bonnet monkeys (Macaca radiata).

Vaccine-associated paralytic poliomyelitis is a serious concern while using the live attenuated oral polio vaccine for the eradication of poliomyelitis. The bonnet monkey model of poliovirus central nervous system (CNS) infection following experimental inoculation into the ulnar nerve allows the comparative study of wild-type and attenuated poliovirus invasiveness. Dosages >/=10(4) TCID(50) of Mahoney strain of poliovirus type 1 [PV1(M)] result in paralysis. In contrast, even with 10(7) TCID(50) of Sabin attenuated strain of poliovirus type 1 (LSc/2ab), no paralysis occurs, but virus spreads into the CNS where viral RNA is found in spinal cord neurons. While wild-type PV1(M) viral RNA replicates in neurons (and possibly in glial cells) and in cells around vessel walls, which may be mononuclear or endothelial cells, attenuated viral RNA is detected only in neurons. Systemic viraemia and gastrointestinal virus shedding occurs only in PV1(M)-infected animals. While a systemic serologic response is detected in both groups of animals, cerebrospinal fluid antibodies are detected only in animals infected with PV1(M). Both the PV1(M) and LSc/2ab strains spread to the cervical spinal cord and then to the lumbar spinal cord following ulnar nerve inoculation. Neuronophagia and neuronal loss are only seen in PV1(M)-infected monkeys in whom clinical paralysis is observed. Infection with LSc/2ab does not result in neuronophagia, neuronal loss or clinical paralysis. Spread of attenuated poliovirus in spinal cord neurons without causing paralysis following inoculation into the ulnar nerve is an important finding.