Abstract

We report a case of Guillain-Barre syndrome (GBS) occurring after measles infection and review the published literature on the subject. A previously healthy 48-year-old man developed fever, cough and constipation, followed by a maculopapular rash over the face and neck. Measles infection was diagnosed. Four days later, he developed back pain and paraesthesias in the hands and feet. Computed tomography, magnetic resonance imaging scans of the brain and a chest radiograph were normal. One day later, he was admitted to hospital for numbness in the hands and feet bilaterally, dyspnoea, perioral pain, headache and nausea. The patient was afebrile and unable to walk and stand upright. He denied prior neurological illnesses. Examination showed weakness of the upper and lower extremities, more pronounced proximally, and symmetrical hypoesthesia. Deep tendon reflexes were absent. Nerve conduction studies showed moderate increase of motor nerve distal latencies, slowing of motor nerve conduction velocity, desynchronization of compound motor action potential amplitudes and reduced amplitude of sensory nerve action potential in the upper limbs. Serum measles IgM antibodies were elevated. Cerebrospinal fluid examination disclosed albumin-cytological dissociation and elevated measles IgM antibody titres. Isoelectric focusing showed a mirror pattern. No paraprotein was found. Antibody titres to cytomegalovirus, rubella, Epstein-Barr virus and herpes simplex viruses 1 and 2 were negative. Anti-ganglioside antibodies were not measured. GBS of the demyelinating type was diagnosed and treatment with intravenous immunoglobulin was given. Over the following three days, the patient developed cranial nerve palsies, tetraplegia, and respiratory insufficiency necessitating admission to the Intensive Care Unit and a tracheotomy. Three weeks later he experienced severe cardiovascular autonomic dysautonomia which resolved within five days. The patient then underwent plasma exchange and began to improve clinically. He was discharged seven weeks after admission, with residual left 7th cranial nerve palsy, severe weakness of foot dorsiflexion, mild proximal muscle weakness of all four extremities, and mild neuropathic pain in the lower limbs. Measles is a vaccine-preventable, acute viral illness which is well-known to cause neurological complications, the most frequent being post-infectious measles encephalitis (PIME). The pathogenetic mechanisms involved in measles neurological complications remain to be completely understood. Interestingly, PIME appears to be caused by an abnormal immune reaction against myelin basic protein and the pathogenesis of GBS also seems to involve an autoimmune-mediated process. Approximately two-thirds of patients with GBS report a preceding infection but the pathogen frequently remains unidentified. Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, Mycoplasma pneumoniae have been shown to be related to GBS and there is some evidence that varicella-zoster and influenza viruses and H. influenzae may also be triggers. A. Filia (&) Infectious Diseases Epidemiology Unit, National Centre for Epidemiology, Surveillance and Health Promotion, Istituto Superiore di Sanita, Viale Regina Elena 299, 00161 Rome, Italy e-mail: antonietta.filia@iss.it

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