Acute motor polyneuropathy as a rare neurological complication of mumps in a child: A case report

INTRODUCTION

A resurgence of mumps outbreaks has been observed in recent times, likely due to waning immunity and suboptimal vaccine coverage. Although mumps is generally a benign and self-limiting viral illness, it remains a notable cause of meningoencephalitis in children. Neurological complications, though rare, may include neuritis, myelitis, hydrocephalus and polyradiculopathy.^[1] We present a rare case of acute motor polyneuropathy developing in a child during the course of mumps infection, highlighting the neurotropic potential of the mumps virus.

CASE REPORT

A 6-year-old developmentally normal male child was brought in with complaints of abdominal pain and progressive weakness of both lower limbs for 10 days. There was a significant history of febrile illness followed by bilateral parotid swelling 10 days before the onset of neurological symptoms.

On examination, the child was conscious, oriented, and haemodynamically stable. General physical examination was unremarkable. Neurological examination revealed lower-limb and truncal weakness with preserved upper-limb and neck-muscle strength [Figure 1]. Deep tendon reflexes were diminished in the lower limbs with a mute plantar response. Cranial nerves and the sensory system were intact, and bladder/bowel functions were normal. Features of meningitis were noted, including neck rigidity and positive Brudzinski and Kernig signs.

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Figure 1: Clinical photographs (a) pre-treatment, (b) post-treatment

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A provisional diagnosis of motor polyneuropathy/Guillain– Barré syndrome (GBS) was made. Cerebrospinal fluid (CSF) analysis showed normal glucose (66 mg/dL) and mildly elevated protein (129 mg/dL) with a normal cell count. Computed tomography of the brain was suggestive of meningitis. Nerve conduction studies demonstrated bilateral ulnar, common peroneal and posterior tibial polyneuropathy [Tables 1 and 2, and Figure 2]. The diagnosis of mumps was supported by the characteristic clinical presentation of fever with bilateral parotid swelling followed by neurological manifestations and was confirmed serologically by detection of mumps-specific IgM antibodies in serum. Buccal swab reverse-transcription polymerase chain reaction (RTPCR) for mumps could not be performed as the child presented in the convalescent phase, after the acute phase of parotitis, and the facility was not available at our centre. Magnetic resonance imaging (MRI) of the brain and spine was attempted but could not be completed as adequate sedation could not be achieved in the child; computed tomography (CT) brain (already obtained) was suggestive of meningitis and there were no clinical features of myelitis (no sphincter involvement, no sensory level, no upper-motor-neuron signs), so MRI was not pursued further after multidisciplinary review.

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Figure 2: Motor nerve conduction waveform tracings for each nerve studied, showing reduced compound muscle action potential (CMAP) amplitudes in the common peroneal (extensor digitorum brevis) recordings (red arrows). Sensory nerve action potentials (SNAPs) over the median and ulnar nerves (upper limbs) and the superficial peroneal and sural nerves (lower limbs) were normal in latency, amplitude and conduction velocity. APB: Abductor pollicis brevis, ADM: Abductor digiti minimi, EDB: Extensor digitorum brevis, AH: Abductor hallucis.

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After multidisciplinary discussion, the patient was managed with intravenous methylprednisolone pulse therapy for 7 days and started on physiotherapy. Intravenous immunoglobulin (IVIG), which is the standard therapy for classical GBS, was not administered because the clinical picture was considered more consistent with post-infectious mumps-associated motor polyneuropathy with concurrent aseptic meningitis rather than classical GBS. The child remained haemodynamically stable throughout, with no respiratory compromise, no cranial nerve involvement, no autonomic instability and no rapidly progressive ascending weakness. The temporal relationship to confirmed mumps infection, the presence of meningitic features and the favourable initial response also supported an immune-mediated, steroid-responsive mechanism. Gradual clinical improvement was noted, with reduced neck rigidity and increased lower-limb activity. The child remained under close observation for any neurological deterioration.

At 6-week post-discharge follow-up, the child had made a complete neurological recovery [Figure 1]. Muscle power had returned to 5/5 in all limbs; deep tendon reflexes were normal; gait and functional mobility were age-appropriate and there were no residual motor, sensory, autonomic, sphincter or respiratory deficits. The child has remained well since, with no relapse or new neurological symptoms at the time of writing.

DISCUSSION

Mumps is a known neurotropic virus and is associated with a wide spectrum of central and peripheral nervous system complications. Meningitis is the most common neurological complication, occurring in 10–30% of symptomatic infections, while asymptomatic CSF pleocytosis may be found in up to 60% of cases.^[2]

Polyneuropathy following mumps is exceedingly rare. The clinical picture in this case initially resembled GBS; however, the presence of recent mumps infection and positive mumps IgM supported a diagnosis of post-infectious mumps-associated polyneuropathy.^[3]

The neuropathogenesis remains poorly understood and may involve immune-mediated demyelination or direct viral injury to peripheral nerves. Further research is required to elucidate the mechanisms of mumps-related peripheral neuropathy.

The choice of intravenous methylprednisolone over IVIG in this case was guided by the clinical phenotype. Although IVIG (or plasma exchange) is the established first-line therapy for classical GBS, our patient presented with a post-infectious motor polyneuropathy occurring in the context of mumps with associated meningitic features, without the rapidly progressive ascending paralysis, respiratory compromise, cranial-nerve involvement or autonomic dysfunction that would typically prompt IVIG. In such immune-mediated, para-infectious presentations with concurrent aseptic meningitis, corticosteroids have been used with favourable outcomes, as observed in our patient. The complete recovery at 6-week follow-up further supports the appropriateness of the treatment strategy adopted.

CONCLUSION

Post-mumps acute motor polyneuropathy is a rare but clinically significant complication of mumps infection in children. A high index of suspicion, supported by serological confirmation of mumps and electrophysiological studies, is essential for early diagnosis and management. This case reinforces the need for universal MMR vaccination and continued vigilance for neurological complications during the convalescent phase of mumps.