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MAY ELECTROPHYSIOLOGY DIFFERENTIATE CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY (CIDP) AND POLINEUROPATHY WITH ANTI‐SGPG ANTIBODIES?
Author(s) -
Capasso M.,
Torrieri F.,
Lugaresi A.,
Uncini A.
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2000.00513-9.x
Subject(s) - polyneuropathy , chronic inflammatory demyelinating polyneuropathy , medicine , antibody , electrophysiology , pathognomonic , nerve conduction , polyradiculoneuropathy , guillain barre syndrome , pathology , immunology , disease
Demyelinating polyneuropathy with anti‐MAG/SGPG ab is elecrophysiologically characterized by a disproportionate distal slowing of motor conductions. A terminal latency index TLI = 0.25 in at least two nerves has been proposed to differentiate polyneuropathy with anti‐MAG/SGPG ab from other chronic demyelinating disorders (Kaku et al. 1994). We reviewed and compared the electrophysiogical studies of 18 patients with CIDP and 8 with polyneuropathy anti‐SGPG antibodies. The Anti‐SGPG group showed: (1) lower CMAP amplitudes and longer motor distal latencies; (2) lower TLI and longer F wave latencies; (3) higher percentages of nerves with TLI = 0.25; (4) much fewer conduction blocks; (5) more frequent absent SAPs. CIDP and polyneuropathy with anti‐MAG/SGPG seems to be, as groups, electrophysiologically different. However, three patients with CIDP showed at least 2 nerves with TLI = 0.25 and one, although displaying all the additional electrophysiological features characteristic of anti‐MAG/SGPG polyneuropathy, was negative for ab search at diagnosis and one year later, and did not have immunoglobulin deposits in sural nerve. On the other hand, one patient with anti‐SGPG antibodies did not have distal disproportionate slowing of motor conduction velocities. In conclusion, demyelination seems to be in anti‐MAG/SGPG polyneuropathy a length‐dependent process, whereas in CIDP it tends to be patchy and multifocal, which strengthens the view that these are two different pathophysiological entities. Electrophysiological findings can suggest an anti‐SGPG polyneuropathy and address the search of ab, but they are not pathognomonic in the individual patient.