Abstract
Guillain–Barré syndrome (GBS) is an acute peripheral neuropathy that develops as a result of post-infectious immune-mediated nerve injury. It can be classified into classic and variant GBS. Acute motor axonal neuropathy (AMAN) is a subtype of GBS with the key clinical features of pure motor weakness, areflexia, absence of sensory symptoms, and lack of neurophysiologic evidence of demyelination. We reported a case of acute motor axonal neuropathy in association with hepatitis E infection. A young woman was referred to us after a period of nausea, fever, and diarrhea. She had unexplained muscle weakness at admission and has been diagnosed with acute hepatitis E infection. A rigorous clinical neurological assessment revealed bilateral symmetrical weakness, which affects the lower limbs more than the upper limbs, with no evidence of sensory involvement. Neurophysiological measurements indicated acute axonal injury without clues to demyelination. A diagnosis of acute motor axonal neuropathy subtype has been made, to which she only received supportive therapy. The symptoms resolved spontaneously and full recovery of motor function was attained after 35 days of weakness onset with complete normalization of neurophysiologic parameters.
Highlights
Guillain–Barré syndrome (GBS) is an acute peripheral neuropathic disease characterized by ascending flaccid paralysis of symmetrical distribution that can present with motor and/or sensory symptoms [1]
We describe a woman with acute pure motor subtype of GBS that has developed in association with hepatitis E infection and recovered spontaneously in parallel with liver functions normalization
Repetitive nerve stimulation targeted to detect deficit associated with periodic paralysis was normal. These findings were consistent with a diagnosis of acute motor axonal neuropathy variant of GBS in association with hepatitis E infection
Summary
Guillain–Barré syndrome (GBS) is an acute peripheral neuropathic disease characterized by ascending flaccid paralysis of symmetrical distribution that can present with motor and/or sensory symptoms [1]. Initial nerve conduction study (NCS) (7 days after the onset of weakness), showed evidence of axonal motor neuropathy of symmetrical distribution affecting the lower limbs more than the upper limbs with normal sensory NCS parameters. Repetitive nerve stimulation targeted to detect deficit associated with periodic paralysis was normal These findings were consistent with a diagnosis of acute motor axonal neuropathy variant of GBS in association with hepatitis E infection (as indicated by the clinical scenario, deranged liver function test, and serological evidence of hepatitis E antibody). Repeated NCS/EMG after 35 days of weakness onset (see Table 1) showed full recovery of motor neurophysiological parameters These changes have been paralleled by clinical improvement in weakness and normalization of liver function test values
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