LETTER TO EDITOR
|Year : 1992 | Volume
| Issue : 1 | Page : 50
Post herpes zoster motor deficit
NR Nagabhushana, BG Ashakiran, DA Satish, Sumathy
N R Nagabhushana
|How to cite this article:|
Nagabhushana N R, Ashakiran B G, Satish D A, Sumathy. Post herpes zoster motor deficit.Indian J Dermatol Venereol Leprol 1992;58:50-50
|How to cite this URL:|
Nagabhushana N R, Ashakiran B G, Satish D A, Sumathy. Post herpes zoster motor deficit. Indian J Dermatol Venereol Leprol [serial online] 1992 [cited 2020 Aug 9 ];58:50-50
Available from: http://www.ijdvl.com/text.asp?1992/58/1/50/3746
To the Editor,
Herpes zoster is primarily a disease of dorsal root ganglion caused by varicella-zoster virus, with inflammation, haemorrhage and infarction. Although the major damage is in the dorsal root ganglion, in many cases the disease spreads to the same segment of the spinal cord, with inflammation, mainly in the posterior and anterior horns and some degree of `destruction of the anterior horn cells with consequent lower motor neurone (LMN) paralysis.  LMN damage may also arise from damage to anterior root where it joins the dorsal root ganglion. 
Broadbent in 1866 first described partial paralysis following zoster.  The occurrence of motor deficit varies from 0.5 percent to 31 percent and is more common in the elderly.  The frequency is 3 times higher with associated malignant disease.  Paralysis of the cranial nerves is not uncommon but spinal nerve root paralysis is rare. Paralysis usually begins within two weeks of the onset of the rash and almost always involves muscle groups with innervation that is contiguous with that of the affected dermatome.  Infrequently, paresis develops before the rash appears. 
A 60-year-old male came to us with the history of groups of painful blisters in the right upper limb 6 months ago. Lesions healed after applying herbal medicines. Two weeks later, he developed weakness in the same limb which persisted without significant change so far. Examination revealed discrete groups of small, hypopigmented scars in the right cervical - 8 and thoracic-1 (C-8 and T-1) dermatomes. He had hypotonia, hyporeflexia, wasting and grade 3 power in the muscles supplied by C-8 and T-1 nerve roots on the right side, suggesting a LMN lesion. There was no motor deficit elsewhere. Sensations were- normal. General and systemic examination revealed no other abnormality.
Radiographs of the spine and neck were normal. Patient was lost for electrophysiological studies and follow up.
The prognosis in cases of motor weakness following herpes zoster is generally good, with 55 percent showing complete recovery and 30 percent significant improvement .The time taken for recovery may range form 3 weeks to 6 months.
|1||Leading Article. Paralysis in herpes zoster. Br Med J 1970; 2:ii: p 379 (Quoted in 2).|
|2||Bradley GB. Myelopathies affecting anterior horn Cells. In : Peripheral neuropathy (Dyck PJ, Thomas PK, Lambert HE, et al eds), 2nd edn. Philadelphia : W B Saunders Company, 1984: 1351 - 67.|
|3||Baringer Jr, Townsend JJ. Herpesvirus infection of the peripheral nervous system. In : Peripheral Neuropathy (Dyck PJ, Thomas PK, Lambert HE, et al eds), 2nd edn. Philadelphia : W B Saunders Company, 1984; 1941 -9.|
|4||Weiss S, Striefer M, Weiser HJ. Motor lesions in herpes zoster. Eur Neurol 1975; 13 : 332.|
|5||Thomas JE, Howard FM. Segmental zoster paresis - a disease profile. Neurol (Minneap) 1972, 22: 459.|
|6||Oxman MN. Varicella and Herpes zoster. In Dermatology in General Medicine (Fitzpatrick TB, Eisen AZ, Wolff K, et al eds), 3rd edn. New York: McGraw-Hill Book Company, 1987; 2314 - 40.|