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Year : 2000  |  Volume : 48  |  Issue : 2  |  Page : 189-90

Herpes zoster cervical myelitis in an immunocompetent subject.

How to cite this article:
Mehndiratta M M, Bansal J, Gupta M, Puri V. Herpes zoster cervical myelitis in an immunocompetent subject. Neurol India 2000;48:189

How to cite this URL:
Mehndiratta M M, Bansal J, Gupta M, Puri V. Herpes zoster cervical myelitis in an immunocompetent subject. Neurol India [serial online] 2000 [cited 2020 Nov 28];48:189. Available from:

Herpes zoster (HZ) results from reactivation of latent infection in the sensory ganglion, established years earlier during the course of primary infection i.e. chickenpox. Although HZ is characteristically benign, however, neurological complications are common and may range from transient pain and paraesthesias associated with the acute rash to post-herpetic neuralgia, segmental sensory loss or motor paresis, encephalitis, myelitis or cerebrovascular manifestations.[1] Clinically, myelopathy is a rare complication and usually it develops in the immunocompromised host. In a large series,[2] the incidence of HZ myelopathy in individuals with compromised immunity has been reported to be around 0.8%. We report a case of cervical HZ myelitis in an immunocompetent young female, who showed complete recovery with parental Acyclovir.
A 35 year old non-diabetic and normotensive female was admitted in September 1994 with vesicular skin eruptions, burning and paraesthesia in the form of pin pricking sensation over back of right shoulder, supraclavicular and infraclavicular regions (in C3, C4 dermatomes) of 3 weeks duration. One week after the appearance of skin rash, she noticed weakness in right hand, which was progressive, and in next four days she developed difficulty in raising right arm above the shoulder. After another four to five days her left hand also became weak. At the same time, she also noticed stiffness and weakness in both lower limbs. During the course of her illness, she never became unconscious or incontinent. She denied any history of prolonged illness or drug intake or contact. Detailed neurological examination revealed asymmetric quadriparesis; upper limbs (right > left) were affected more than the lower limbs. Power was grade 3/5 in right upper limbs and 4+/5 in all other limbs. All deep tendon reflexes were brisk with extensor plantars. There was partial loss of touch, pain and temperature sensation below C4 dermatome. Scabs were observed over C3-C4 dermatome on right side. There was no tenderness or deformity of spine. Rest of systemic examination was essentially normal.
Routine investigations including haemogram, liver function tests, kidney function tests, blood sugar and X-rays chest were normal. Enzyme linked immunosorbent assay (ELISA) for human immunodeficiency virus (HIV) was negative and VDRL was non-reactive. Differential lymphocyte cell count (CD4/CD8) was normal. CSF protein was mildly raised (60mg%) with normal sugar level. Magnetic Resonance Imaging (MRI) T1, T2 and proton density images, sections showed generalized swelling and enlargement of the spinal cord at C2-C5 level. T1 weighted images revealed hypo-intense signals in the same region. There was mild patchy enhancement with gadolinium. The cranio-vertebral junction was normal. MRI findings were suggestive of transverse myelitis. Patient was given parental acyclovir (500mg, 8 hourly for 10 days). She started improving on the third day of acyclovir administration and within 4 weeks she recovered completely. There was no history of development of any other opportunistic illness during last 5 years follow up.
Hardy first reported Herpes zoster myelitis (HZM) in 1876.[1] HZM is usually unilateral and if bilateral, is asymmetric. Devinsky and colleagues[1] analysed their findings in 38 immuno-compromised patients with HZM. HZM is considered to be very rare in patients with preserved immunity. The syndrome of progressive myelopathy without evidence of encephalopathy in association with HZ is quite rare.[3]
Magnetic Resonance Imaging (MRI) is a sensitive and quite specific tool of investigation for diagnosis of myelitis.[4] MRI not only provides information about the site but also the extent of involvement of spinal cord. In our patient, the cervical cord was swollen with altered signal intensity from C2 to C5 segments. Cervical myelitis is reported to be very uncommon.[1],[4] Devinsky et al observed quadriparesis in 3 subjects only among 13 cases reported by them as well as 25 previously documented cases. The average latent period between onset of rash and the appearance of myelitis is 8.5 days with a range of 5-10 days.[1] In our patient described above, myelopathy occurred 7 days after the onset of rash. To the best of our knowledge, there are only five cases reported earlier from India,[5],[6] but all these cases manifested as paraparesis, while the present case had quadriparesis. Prognosis is good with partial or complete recovery. With the advent of acyclovir, the outlook of patients affected by this disease has further improved. With the increasing incidence of HIV infection, the incidence of HZ infection and its neurological complications is increasing. A prophylactic use of acyclovir should best be restricted to immuno-suppressed individuals who are at high risk.


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1.Devinsky O, Cho ES, Petito CK et al: Herpes zoster myelitis. Brain 1991; 114:1181-1196.   Back to cited text no. 1    
2.Schimpff S, Serpick A, Stoler B et al: Varicella-Zoster infection in patients with cancer. Ann Inter Med 1972; 76: 241-254.   Back to cited text no. 2    
3.Hogan EL, Krigman MR: Herpes zoster myelitis: Evidence for viral invasion of spinal cord. Arch Neurol 1973; 29: 309-313.   Back to cited text no. 3    
4.Hirai T, Korogi Y, Hamatake S et al: Varicella zoster virus myelitis-serial MRI findings. Br J Radiol 1996; 69: 1187-1190.   Back to cited text no. 4    
5.Panagariya A, Bhargava A: Transverse myelitis-an unusual complication of Herpes zoster. Neurol India 1993; 41: 117-118.   Back to cited text no. 5    
6.Sharma R, Vijayvergiya R, Baid CS et al: Zoster myelitis and its response to acyclovir. J Assoc Physicians India 1996; 44: 220-221.   Back to cited text no. 6    


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