Herpes Zoster Confused with Radiculopathy Young-Joon Ahn, M.D.,* Changju Hwang, M.D., Kyeong-Il Jeong, M.D.,† Sung-Woo Lee, M.D., Yung-Tae Kim, M.D., Dong-Ho Lee, M.D. It was reported that the doctor feels it is herpes zoster. The patient was given unspecified treatment. Moreover, a case of BSS after infection with Borrelia burgdorferi responded to antibiotic treatment.2 Until now, the only association of virus infection with BSS is brief mention of an incomplete BSS (weak left leg with an extensor response and decreased sensation over the right leg) after T12-distribution zoster3 and features of BSS with varicella zoster virus (VZV) meningoencephalomyelitis and vasculitis.4 Here we report a case of BSS after reactivation of VZV. Patellofemoral Brace. The patient received intravenous acyclovir 750 mg/day for 7 days and continued to take the prednisolone. Unnecessary treatments including surgery should be avoided by early, correct diagnosis through prudent history taking and physical examination.
The rarest sites of zoster were the lower lumbar and sacral dermatomes. The patient was previously healthy, circumcised, and fully immunized through the age of two to include varicella. The velocity at which varicella zoster virus (VZV) travels in a human neuron has never been determined. The severe combined immunodeficient mouse with explants of human tissue is the best available animal model for VZV infection . However, there is no ideal animal model that fully replicates all the features of VZV reactivation from latency and subsequent anterograde spread of virus. Anti-varicella-zoster virus immunoglobulin (Ig) M antibody was not detected, and the IgG antibody titer did not increase. Recently, we observed a child who had developed shingles of the foot.
Then the patient starts to feel numbness, tingling, burning, itching or pain in the dermatome (area of the skin, supplied by a nerve) affected. Administered by: Private Purchased by: Private Symptoms: Erythema, Herpes zoster, Hypotonia, Infection, Pruritus, Rash vesicular Write-up: Generally healthy 3 yo male developed vesicular rash on L knee which spread rapidly up thigh, hip, buttocks. There are also a few vesicular lesions just by the nipple level as well and when you look at he back a similar lesion was also on the same dermatome about T5 and 6 posteriorly but did not cross the midline. There really was not significant parenthesias on it, the patient did not complain of any pain over it either. As people age, their spines are subject to increasing degeneration which can cause herniated discs and similar problems, leading to lumbar radiculopathy. This was not the case with this patient. Symplex 1 I think is oral herpes.
This is in follow-up to report(s) previously submitted on 5/16/2005. Histopathologic examination of lesional skin biopsy revealed an intense mononuclear cell infiltration with many eosinophils and an interface dermatitis with hydropic degeneration of basal keratinocytes, while in the spared area, only slight lymphocytic infiltration was present in a perivascular distribution. There were no adverse events following prior vaccination. No further information is expected. Of note, he had received a diagnosis of acute lymphocytic leukemia at age 4 years. He had responded well to both induction and maintenance chemotherapy and was now in remission. At the time of admission, he was not receiving any chemotherapy.
Nevertheless, the history of leukemia prompted the current admission. During examination, the child appeared to be well nourished and well developed. Based on these findings a conservative treatment including oral analgesia, physiotherapy and a series of lumbar epidural corticosteroid infiltrations was initiated. This patient was a 19 month old previously healthy child that developed a dermatomal rash in her right upper extremity at the site of her prior vaccination at 15 months. Herpes zoster developed in 8 patients at a median of 12 months post transplant, while 10 patients presented with late onset hemorrhagic cystitis at a median of 35 days post transplant. He was able to move his quadriceps, hamstrings, gastrocnemius, soleus, tibialis anterior, extensor hallucis longus, and flexor hallucis longus muscles in both legs. However, he was unable to stand because of exquisite pain in his left lower back and left leg.
He stated that any movement of the left leg led to substantial pain in the left flank. There was no recent exposure of chicken pox or herpes zoster. CT of the lower spine, pelvis, and legs detected no boney abnormalities or soft tissue swelling. Abdominal plain films were read as normal. No evidence for relapse of leukemia was discovered after an extensive hematologic evaluation. On the evening of the patient’s third day in the hospital, 6 December, a vesicular rash erupted over the medial side of his left foot (Figure 1). A scraping was obtained for examination by an immunofluorescent rapid VZV diagnostic test.
The cells stained positively for VZV antigens. The diagnosis of zoster of the left foot was made. The child immediately began receiving treatment with intravenous acyclovir (30 mg/kg/day), followed by treatment with oral acyclovir after discharge from the hospital. He had a complete recovery without postherpetic neuralgia. He was well at a 1-year follow-up examination, without any relapse of leukemia. Exanthem on medial side of left foot. Cells were obtained from the fluid in the vesicular exanthem and examined for varicella zoster virus (VZV) and herpes simplex virus (HSV) antigens.
The VZV antigen test result was positive, and the HSV antigen test result was negative. Of note, the boy had never received the live attenuated varicella vaccine at age 1 year. The physician treated the patient with acyclovir 200 mg/5 ml”s for 20 mg/kg, four times a day, about 4 teaspoons four times a day, told her to keep it covered, may wash it with soap and water, try not to be expose anyone who hasn”t had chickenpox or shingles “because they will surely get this”. The virus lies dormant in the majority of people”s nerve cells for a lifetime. Because of the history of acute leukemia, the mother had become an excellent historian. She was clearly aware of the timing of the first complaints of pain in the lower back by her son. No product quality complaint was involved.
Therefore, we consider the painful episode to be an accurate indicator of VZV replication in the lumbosacral ganglion. Because the VZV replication cycle is ∼16 h , we cannot exclude the possibility that the onset of zoster was actually a day earlier than the onset of pain. We consider the zoster episode to be linked to prior chemotherapy. Before the approval of varicella vaccination in 1995, we conducted a prospective 9-year survey of zoster in all our children receiving treatment for acute lymphocytic leukemia . During the 9 years, a total of 14 children manifested 17 episodes of zoster. Almost 75% of the episodes occurred within the first 2 years after diagnosis of leukemia. However, a few cases extended to 65 months after diagnosis of leukemia, a period similar to the current case.
The sciatic nerve is the longest nerve in the human body . Movement and sensation in the legs and feet are largely dependent on normal functioning of the sciatic nerve. After supervising the care of this child, we surmised that we had a singular opportunity to calculate the velocity of the VZ virion in a human nerve. The authors describe this case because zoster paresis should be one of the differential diagnoses of girdle muscle weakness and because the rash followed the leg paresis. This rash was in the L4 dermatome . If the sciatic nerve is assumed to be ∼80 cm in this child , then the VZ virions would have traveled 800 mm in 6 days, or 133 mm in 1 day. This corresponds to a rate of 5.55 mm/h, or .092 mm/min or .0015 mm/s (1.5 μm/s).
If we allow 1 extra day for viral replication in and initial transit from the lumbosacral ganglion before onset of symptomatic ganglionitis, the VZ virions would have traveled 800 mm in 7 days, or 114 mm in 1 day. This velocity corresponds to .0013 mm/s (1.3 μm/s). In summary, this uncommon case of sciatic zoster is an experiment of nature that provides considerable insight into the anterograde transit time of the varicella zoster virus in a sensory human neuron during clinical zoster. This transit time overlaps with that of the closely related PRV, when examined in an animal model. In the PRV laboratory, the investigators calculated an anterograde velocity of 1.97 μm/s and a retrograde velocity of 1.28 μm/s for PRV when traveling in sensory axons removed from embryonic chick embryos . In an earlier study, investigators studying HSV-1 in the giant axon of the squid estimated a retrograde velocity of 2.2 μm/s . In one sense, therefore, the human zoster case validates that the fast-axonal transport mechanism proposed for herpesviruses in 2 widely divergent animal models can be applied to VZV transportation in human neurons .