Herpes zoster is a common viral disease due to reactivation of a latent varicella zoster virus in the dorsal sensory ganglia. It is responsible for a wide variety of neurological manifestations, but motor neuropathy is an uncommon complication. The incidence of this complication is reported to be between 0.5-31%, but particularly when the eruption is peripheral, the situation in which motor loss may occur is only 1-5% of cases. But recent objective studies using electromyography or a motor nerve conduction velocity test have reported a higher incidence of motor nerve abnormalities. Haanpaa et al. reported that the incidence of herpetic motor paresis was 17.5% and abnormalities of electromyography were 53% and they found little correlation between motor loss severity and pain severity. This suggested there are many patients who have subclinical motor nerve abnormalities.
Motor nerve abnormalities caused by herpes zoster can occur in both visceral and somatic (cranial and peripheral) nerves. Sites of involvement, in descending order of frequency, are the thorax, neck, face, cervical, and lumbosacral area. Although the thoracic region is the most common site, a patient presenting with segmental paresis is rare. The highest rate of occurrence is found in facial paralysis following cranial herpes zoster, such as Ramsay Hunt and Horner syndromes.
The distribution of the weakness is usually segmental, occurring in the same myotomes as the involved or adjacent dermatomes. Segmental zoster paresis usually affects the upper limbs more than the lower limbs. Electromyographic abnormal findings in zoster-induced paralysis can show fibrillation potential, positive sharp waves, bursts of high frequency discharge, polyphasic motor unit potential, fasci- culation, and increased insertional activity of involved muscles. A motor nerve conduction velocity test can also show a variable degree of an abnormal latency period, amplitude, and conduction velocity of involved muscles. But there is no association between severity of rash, pain and EMG abnormalities.
The interval between the appearance of a rash and the onset of muscle weakness varies. It most commonly occurs within days of the cutaneous rash, but a delay of several months has also been reported. And there are cases of zoster-induced paresis preceding the skin lesions.
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The exact pathogenesis of muscular paralysis following herpes zoster infection remains unclear, but it is generally accepted that motor paralysis results from viral spread from the dorsal root ganglion to the anterior horn cells or anterior spinal nerve roots, progressive hypersensitivity to VZV antigen, inflammation along the mixed motor and sensory tract, and secondary degeneration in the affected motor neurons.
In the study by Mondelli et al., motor loss and electromyographic evidence of axonal damage were less marked among 47 patients who were treated with acyclovir (4 g/d) than among patients who did not receive antiviral therapy. Antiviral therapy may improve the clinical outcomes by reducing peripheral sensory axonopathy and preventing viral spread. Physical therapy prevents from contracture and atrophy of involved muscles, which causes permanent loss of motor function, even though the exact mechanism and rationale of this in motor paralysis caused by herpes zoster is uncertain.
Overall prognosis of zoster-induced motor paralysis is favorable. A literature review by Merchut and Gruner indicated that 74% of patients recovered normal motor function, within 20 months on average (range, 2-108 months). Similarly, Haanpaa et al. reported 70% of cases have complete functional recovery and about 20% of cases have partial recovery or permanent residual deficits. Electrophysiological studies have confirmed complete denervation of muscle with delayed reinnervation. This suggests that recovery depends on axonal regeneration from a proximal site. Motor neuron cell death may explain the poor prognosis of some casesof herpes zoster. Magnetic resonance imaging (MRI) evidence of glial scar formation in the cervical cord has been reported in one patient following resolution of post-herpetic polyradiculitis. It may explain the reason that up to one third of patients do not have a complete recovery.
To date, 6 cases of motor paralysis after herpes zoster have been reported in the Korean dermatologic literature (Table 2). The ages range from 65-81 years, with the average of 71.83 years. The lesions were distributed as follows: 2 cases on the abdomen, 2 cases on the arm, one case on the leg and one case on the face. Two cases of motor paralysis did not improve at all. Two cases involving the arm were similar to our case due to their site and extent.
In the present case, the patient motor activity improved to some degree. There have been some cases of segmental motor paralvsis caused by herpes zoster without improvement. So we suggest that dermatologists should bear in mind the possibility of motor nerve deficit with herpes zoster.