OBJECTIVES: Patients with polyneuropathy and antibodies to myelin-associated glycoprotein (MAG) and sulphated glucuronyl paragloboside (SGPG) differ from chronic inflammatory demyelinating polyneuropathy (CIDP) because of a slower, progressive course, symmetrical and predominantly sensory involvement of legs, predominantly distal slowing of motor conductions, and poorer response to therapy. We studied whether a wide set of electrophysiologic parameters may differentiate these two neuropathies. METHODS: We reviewed the electrophysiological studies of 10 patients with anti-MAG/SGPG antibodies and 22 with CIDP examining: (1) motor conduction velocity and distal compound muscle action potential amplitude; (2) conduction block (CB) and temporal dispersion; (3) distal motor latency and terminal latency index (TLI); (4) F wave and proximal conduction time; and (5) sensory conduction and occurrence of abnormal median with normal sural sensory potential. RESULTS: Anti-MAG/SGPG neuropathies showed: (1) more severe involvement of peroneal nerves; (2) more frequent disproportionate distal slowing of motor conductions (TLI< or =0.25) and absent sural potential, and (3) no CB. However 3/22 CIDP patients also had at least two nerves with TLI< or =0.25 and no CB. CONCLUSIONS: Electrophysiologic findings suggest in anti-MAG/SGPG neuropathy a length-dependent process with a likely centripetal evolution. A disproportionate slowing of conduction in distal segments of motor nerves suggests the diagnosis of anti-MAG/SGPG neuropathy, although it is not pathognomonic.
OBJECTIVES:Patients with polyneuropathy and antibodies to myelin-associated glycoprotein (MAG) and sulphated glucuronyl paragloboside (SGPG) differ from chronic inflammatory demyelinating polyneuropathy (CIDP) because of a slower, progressive course, symmetrical and predominantly sensory involvement of legs, predominantly distal slowing of motor conductions, and poorer response to therapy. We studied whether a wide set of electrophysiologic parameters may differentiate these two neuropathies. METHODS: We reviewed the electrophysiological studies of 10 patients with anti-MAG/SGPG antibodies and 22 with CIDP examining: (1) motor conduction velocity and distal compound muscle action potential amplitude; (2) conduction block (CB) and temporal dispersion; (3) distal motor latency and terminal latency index (TLI); (4) F wave and proximal conduction time; and (5) sensory conduction and occurrence of abnormal median with normal sural sensory potential. RESULTS: Anti-MAG/SGPG neuropathies showed: (1) more severe involvement of peroneal nerves; (2) more frequent disproportionate distal slowing of motor conductions (TLI< or =0.25) and absent sural potential, and (3) no CB. However 3/22 CIDPpatients also had at least two nerves with TLI< or =0.25 and no CB. CONCLUSIONS: Electrophysiologic findings suggest in anti-MAG/SGPG neuropathy a length-dependent process with a likely centripetal evolution. A disproportionate slowing of conduction in distal segments of motor nerves suggests the diagnosis of anti-MAG/SGPG neuropathy, although it is not pathognomonic.
Authors: T Levine; A Pestronk; J Florence; M T Al-Lozi; G Lopate; T Miller; I Ramneantu; W Waheed; M Stambuk; M J Stone; R Choksi Journal: J Neurol Neurosurg Psychiatry Date: 2006-02 Impact factor: 10.154
Authors: Christopher J Klein; Joon-Shik Moon; Michelle L Mauermann; Steven R Zeldenrust; Yanhong Wu; Angela Dispenzieri; Peter J Dyck Journal: Can J Neurol Sci Date: 2011-03 Impact factor: 2.104
Authors: Pierre Lozeron; Vincent Ribrag; David Adams; Marion Brisset; Marguerite Vignon; Marine Baron; Marion Malphettes; Marie Theaudin; Bertrand Arnulf; Nathalie Kubis Journal: J Neurol Date: 2016-06-17 Impact factor: 4.849