A Case of Acute Motor and Sensory Axonal Neuropathy Following Hepatitis A Infection
A 21-yr-old male was transferred to our hospital due to respiration difficulties and progressive weakness at 16th July 2010 from a local hospital where the patient had been admitted after a 7-day history of symptoms of acute viral hepatitis. In addition, the patient did not have a past history of respiratory or gastrointestinal infection within 1 month before onset of progressive weakness. Physical examination upon referral to our hospital showed the patient presented with anorexia, jaundice, and elevated transaminase levels (serum glutamic oxaloacetic transaminase, 385 IU/L; serum glutamic pyruvic transaminase, 376 IU/L). Immunoglobulin M (IgM) antibodies against HA were detected in blood and cerebrospinal fluid (CSF). Based on impaired liver function tests, clinical features, and the presence of anti-HA IgM antibody; the absence of markers for hepatitis B, C, D, E, diagnosis of acute HA was established. CSF analysis showed protein, 156 mg/dL; glucose, 61 mg/dL, with no pleocytosis. Results of serological and CSF tests for C. jejuni, cytomegalovirus (CMV), Epstein-Barr virus (EBV) and Haemophilus influenzae (H. influenzae) infection were negative. Anti-GQ1b and GM1 antibodies were not found in serum. An abdominal ultrasound showed altered echotexture of liver parenchyma. On neurological examination, the mental status of the patient was alert. By the Medical Research Council (MRC) grading, the patient had weakness with areflexia in both proximal upper limbs (MRC grading 4), both distal upper limbs (MRC grading 2), both proximal lower limbs (MRC grading 4), and both distal lower limbs (MRC grading 2). Pin-prick, vibratory, and joint position senses were reduced in glove and stocking distribution. Nerve conduction studies (NCSs) were performed at 2 weeks after the onset of weakness. The findings of motor NCSs showed markedly reduced amplitudes of CMAPs whereas distal latencies and motor conduction velocities were normal in bilateral peroneal, and posterior tibial nerves, without evidence of demyelination. The findings of sensory NCSs revealed decreased amplitudes of SNAPs and normal conduction velocities in bilateral median, ulnar, and sural nerves (). F-wave response was absent in the right median and both peroneal nerves. The needle electromyography examination demonstrated markedly abnormal reduction in recruitment, with positive sharp waves in the bilateral tibialis anterior and peroneus longus muscles. Based on clinical features with motor and sensory involvement, laboratory findings and electrophysiologic investigation, this patient was diagnosed the AMSAN subtype of GBS following acute HA viral infection according to proposed diagnostic criteria of GBS (). The patient was treated with 0.4 mg/kg/day of intravenous immunoglobulin for 5 days and recovered slowly. Four months later, the patient continued to exhibit marked wasting and weakness of the distal upper and lower limb muscles.