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The muscle findings in a pediatric patient with live attenuated oral polio vaccine-related flaccid monoplegia
Author links open overlay panelShin-ichiUchiyamaa
IchizoNishinobTatsuroIzumia
doi.org/10.1016/j.vaccine.2014.07.089
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Highlights

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We examined a pediatric patient who was given live-attenuated oral polio vaccine.
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He presented limp at 3 years, without distinct gait disturbance during infancy.
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MRI revealed multiple crack-lines in the left anterior tibial muscle.
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Electromyography showed continuous fibrillation potentials.
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Muscle biopsy revealed to be nearly normal histology.

Abstract

A pediatric patient, who was given live-attenuated oral polio vaccine twice without distinct gait disturbance during infancy, begun to present limp at 3 years. His gait disturbance became remarkable with aging. At 7 years, he was unable to dorsiflex the left ankle, and presented flaccid monoplegia of the left lower extremity, and the left Achilles tendon reflex was diminished. Magnetic resonance imaging revealed multiple crack-lines in the left anterior tibial muscle, but was unable to detect any distinct lesion at responsible level of L4, L5 and S1 anterior horn cells’ degeneration. Electromyography showed continuous fibrillation potentials, but muscle biopsy presented nearly normal in this muscle. The serum levels of polio antibody type 1 and type 2 titers were elevated 64× respectively, while the type 3 antibody titer was not elevated 4×. This patient was diagnosed as live attenuated oral polio vaccine-related flaccid monoplegia, with mild clinical course.

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Keywords
Live attenuated oral polio vaccine
Flaccid monoplegia
Mild clinical course
Muscle biopsy
Magnetic resonance imaging
Electromyography
1. Introduction

Acute flaccid monoplegia is an usual and rare condition. In Japan, live-attenuated vaccine-related paralytic polio has been reported to present with a frequency of one in every 4.4 million vaccinated children almost every year. Herein, we described a pediatric patient who had present very mild clinical course of flaccid monoplesia and delayed diagnosis, and his unique muscle findings.
2. Case report

A pediatric patient, who consulted to our hospital for the first time at 7 years 11 months, begun to present limp when he ran at around age of 3 years and 6 months. His gait disturbance was mild and not conspicuous while he moved and took active playing in daily life during infancy. His past-history of gestational, perinatal, neonate, and infancy were uneventful. He was a third product of non-consanguineous healthy Japanese parents. Developmental milestones were also normal, such as head control, sit and walk alone at 3, 7 and 10 months old, respectively. Live attenuated oral polio vaccine was given twice at age of 3 and 6 months. This patient might have mild symptoms of vaccination related paralytic polio in the affected limp that went unnoticed until 3 years old. Other vaccinations had also been given according to the immunization schedule for children, including BCG vaccination at 5 months, DPT at 6, 7 and 8 months, and MR vaccine at 1 year and 7 months.

These vaccinations were done uneventfully.
3. Findings on admission

The patient presented drop foot, flaccid monoplegia, on left foot. On his left big toe, he could do it plantar-flexion, but impossible dorsi-flexion. The 2nd to 5th toes could not present planter-flexion or dorsi-flexion. The localized atrophy of left anterior tibial muscle was distinct and its left Achilles tendon reflex was diminished. Other deep tendon reflexes, including patellar tendon reflex, were all normal brisk responses, without any asymmetrical response. The serum levels of serum polio viral antibody type 1 and 2 titers were elevated to 64× each, whereas a less than 4-fold of the type 3 antibody titer was observed. The CSF chemistry and cytology were all normal ranges. The CSF polio antibody titer less than 1-fold for all of the antibodies types 1–3. MRI of the lower legs revealed localized atrophy and multiple crack-lines in both of the left anterior tibial muscle and toe extensor muscle (Fig. 1). Needle electromyography showed continuous fibrillation potentials in both of left anterior tibial muscle (L4–5, deep peroneal nerve) and left extensor hallucis longus muscle (L5–S1, deep peroneal nerve). MRI could not detect any anterior horn cell's degeneration in spinal cord at the responsible level of L4, L5 and S1. Biopsied muscle finding from the left anterior tibial muscle showed mild grouped variation in the muscle fiber diameters (Fig. 2). Although there was mild atrophy of the type 2 fibers on routine ATPase staining (Fig. 3), these changes were mild, without any findings such as small grouped atrophy in that of Werdnig–Hoffman disease.

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Fig. 1. MRI; localized multiple muscle crack-lines in lt. Anterior tibial muscle. MRI of the lower legs revealed localized atrophy and multiple muscle crack-lines both of the left anterior tibial muscle and toe extensor muscle.

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Fig. 2. Needle electromyography in left anterior tibial muscle (L4–5, deep peroneal nerve). It showed continuous fibrillation potentials and positive sharp wave.

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Fig. 3. Biopsied muscle pathology of lt. anterior tibial muscle in H–E and the routine ATPase staining. It presented mild fiber size differences among muscle fiber groups. The routine ATPase staining presented mild type 2 muscle atrophy.
4. Discussion

A pediatric patient was found to have flaccid monoplegia of the left lower extremity and atrophy both of the anterior tibial muscle and extensor hallucis longus muscle, at the level of the left anterior horn cells at L4, L5, and S1, after lived-attenuated oral polio vaccine inoculation twice. EMG revealed continuous fibrillation potentials from these muscles, and MRI showed localized atrophy and multiple crack-lines in these muscles, but could not detect any distinct lesion at responsible level of L4, L5 and S1 anterior horn cells of spinal cord. Muscle biopsy from left anterior tibial muscle presented nearly normal, except mild group variation in muscle fiber diameters. Based on the finding of elevated serum titers of polio virus type 1 and type 2 antibodies, the patient was diagnosed as having lived attenuated polio vaccine-related flaccid monoplegia. Because of bifurcating axons from adjoining anterior horn cells, reinnervation of the denervated muscles, originally from L4, L5, and S1, might regenerate these muscle fibers. MRI revealed the inflammation area of affected anterior horn cells in the spinal cord during acute phase of polio-vaccine related monoplegia. Because of the small and localized lesion and long history after the real onset. We could not detect the distinct denervated lesion after the recovery phase in this patient, later than 7 years and more, even with 3.0 Te MRI [1], [2]. Because of the small and localized lesion, this patient could not detect a distinct MRI finding of the denervated lesion of spinal cord after the recovery phase. Other differential diagnosis was limited in such as enterovirus or herpes type 1 infection, Hopkins syndrome, transverse myelitis, acute disseminated encephalitis/multiple sclerosis, malignant lymphoma, localized bleeding from an arteriovenous malformation of the spinal cord, and unilateral or localized lesions of the peripheral nerves or muscles, which were all excluded by the clinio-laboratory examinations. It may be highly likely that this patient will present the progress of muscle atrophy as postpolio syndrome with aging and daily active use, here after.

In Japan, vaccine-related paralytic polio has been estimated to occur at a frequency of one in every 3.7 million vaccinated children [3]. In this patient, because of mild and localized lesions, the acute phase of the disease went through unnoticed, and then the pathological changes came to be remarkable through 3–4 years later. The diagnosis was established 7 years later. Acute flaccid monoplegia is an unusual condition associated with only limited diseases such as polio, enterovirus infection, transverse myelitis, malignant lymphoma, localized bleeding from an arteriovenous malformation of the spinal cord, and unilateral or localized lesions of the peripheral nerves or muscles. A physical finding, clinical history taking, CT/MRT of the affected muscles, and electromyography were useful for establishing the diagnosis in this patient.

There were neither distinct laboratory findings nor clinical signs of immune deficiency in this patient after the recovery phase, who received the first inoculation of live attenuated oral polio vaccine at 3 and 6 months after birth, and subsequently also received subcutaneous inoculation of DPT vaccine in the right, left and right upper limbs at 8, 11 and 15 weeks of age, respectively. It might be a risk factor, because subcutaneous or intramuscular injection and needle electromyography around the period of exposure to polio virus might activate the pathway of infection. Dental extraction, tonsillectomy, surgery, and intramuscular injections within 1 month of administration of liver oral polio vaccine have also been reported to serve as risk factors for the development of vaccine-related polio, highlighting the need for attention to be paid to avoid these procedures in the immediate period following oral polio vaccination [4], [5], [6], [7].
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