Thirugnanam Umapathi1, Zongbin Li2, Kamal Verma3, Nobuhiro Yuki4. 1. Department of Neurology, National Neuroscience Institute, Singapore. Electronic address: umapathi@nni.com.sg. 2. Yong Loo Lin School of Medicine, National University of Singapore, Singapore. 3. Department of Neurology, National Neuroscience Institute, Singapore. 4. Departments of Medicine and Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Abstract
OBJECTIVE: The "sural-sparing pattern" of Guillain-Barré syndrome (GBS) is believed to reflect demyelinating pathology. We asked if it is present in non-demyelinating GBS-subtypes, namely acute motor axonal neuropathy (AMAN), acute motor-sensory axonal neuropathy (AMSAN) and Miller Fisher syndrome (MFS), in addition to acute inflammatory demyelinating polyneuropathy (AIDP). METHODS: We studied the occurrence of sural-sparing pattern in clinically defined GBS and MFS patients. Using serial electrodiagnostic studies, GBS patients were divided into AIDP, according to appearance of demyelination-remyelination and AMAN/AMSAN, if there were signs of reversible conduction failure or Wallerian-like degeneration. Equivocal cases were left unclassified. We defined sural-sparing as a greater decrease in median and or ulnar sensory nerve action potential than that of the sural, compared to age and height-matched normal controls. RESULTS: Twelve of 30 GBS and 7 of 20 MFS patients had sural-sparing. This pattern was seen in 4 of 8 AIDP, 5 of 13 AMAN/AMSAN and 3 of 9 unclassified cases. Sequential studies uncovered sural-sparing, initially covert, in additional 1 MFS, 1 unclassified, 1 AIDP and 1 AMAN/AMSAN patient. CONCLUSIONS: Sural-sparing occurs in axonal and demyelinating GBS subtypes. SIGNIFICANCE: The sural-sparing pattern reflects a pathological process common to axonal and demyelinating GBS-subtypes alike.
OBJECTIVE: The "sural-sparing pattern" of Guillain-Barré syndrome (GBS) is believed to reflect demyelinating pathology. We asked if it is present in non-demyelinating GBS-subtypes, namely acute motor axonal neuropathy (AMAN), acute motor-sensory axonal neuropathy (AMSAN) and Miller Fisher syndrome (MFS), in addition to acute inflammatory demyelinating polyneuropathy (AIDP). METHODS: We studied the occurrence of sural-sparing pattern in clinically defined GBS and MFSpatients. Using serial electrodiagnostic studies, GBSpatients were divided into AIDP, according to appearance of demyelination-remyelination and AMAN/AMSAN, if there were signs of reversible conduction failure or Wallerian-like degeneration. Equivocal cases were left unclassified. We defined sural-sparing as a greater decrease in median and or ulnar sensory nerve action potential than that of the sural, compared to age and height-matched normal controls. RESULTS: Twelve of 30 GBS and 7 of 20 MFSpatients had sural-sparing. This pattern was seen in 4 of 8 AIDP, 5 of 13 AMAN/AMSAN and 3 of 9 unclassified cases. Sequential studies uncovered sural-sparing, initially covert, in additional 1 MFS, 1 unclassified, 1 AIDP and 1 AMAN/AMSAN patient. CONCLUSIONS: Sural-sparing occurs in axonal and demyelinating GBS subtypes. SIGNIFICANCE: The sural-sparing pattern reflects a pathological process common to axonal and demyelinating GBS-subtypes alike.