The F wave disappears due to impaired excitability of motor neurons or proximal axons in inflammatory demyelinating neuropathies. Issue 6 (June 1996)

• Record Type: Journal Article
• Authors: Yokota, T; Inaba, A; Yuki, N; Ichikawa, T; Tanaka, H; Saito, Y; Kanouchi, T
• Is Part Of: Journal of neurology, neurosurgery and psychiatry. Volume 60:Issue 6(1996)
• Page Start: 650
• Page End: 654
• Publication Date: 1996-06
• Subjects: Neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; Psychiatry -- Periodicals; 616.8
• DOI: 10.1136/jnnp.60.6.650
• Languages: English
• ISSNs: 0022-3050

Abstract

Abstract : OBJECTIVES--Investigation of pathophysiology of F wave disappearance in demyelinating neuropathies. METHODS--The peripheral motor nerve conduction was studied by motor evoked potential (MEP) on transcranial magnetic stimulation as well as conventional nerve conduction studies before and after the treatment in 26 patients with inflammatory demyelinating neuropathies. In addition, serum antiganglioside antibodies in the acute or active stage were examined. RESULTS--The F wave was abolished in 10 patients. Seven of the 10 patients showed motor evoked potentials (MEPs) on transcranial magnetic stimulation that ranged from 1-4 mV. In six of them the F wave reappeared in the recovery stage, but the MEP size did not change. This may be caused by humoral factors, because the F wave reappeared immediately after plasma exchange or intravenous immunoglobulin treatment. A correlation of F wave disappearance with the presence of serum antiganglioside antibodies was found. CONCLUSIONS--The major pathophysiology of F wave disappearance in demyelinating neuropathies is impairment of motor neuron excitability or prolonged refractoriness of the most proximal axon for backfiring. The conventional interpretation that absent F waves suggest a conduction block at the proximal site is often inadequate.