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Severe degeneration of peripheral motor axons after spinal cord injury: A European multicenter study in 345 patients


Van De Meent, H; Hosman, A Jf; Hendriks, J; Zwarts, M; Schubert, M (2010). Severe degeneration of peripheral motor axons after spinal cord injury: A European multicenter study in 345 patients. Neurorehabilitation and Neural Repair, 24(7):657-665.

Abstract

OBJECTIVE: . There are indications that perilesional and remote peripheral motor axons may degenerate after spinal cord injury (SCI). The authors investigated the magnitude and dependence on severity of SCI of this degeneration as well as whether motor axons so affected can recover. METHODS: . The function of the peripheral motor axons was investigated by recording compound muscle action potentials (CMAPs) in 345 patients with cervical SCI. CMAP amplitude changes in the abductor digiti minimi (ADM) and abductor hallucis (AH) muscles were investigated in 3 groups with SCIs of differing severity: patients with permanent complete SCI (ASIA Impairment Scale [AIS] A-remain), patients with initially complete SCI converting to incomplete lesion(AISA-convert), and patients with incomplete injury (Incomplete). RESULTS: . Significant decreases in ADM and AH CMAP amplitudes were found in groups A-remain and A-convert. In group A-remain and group A-convert, the authors found a partial, although significant, recovery of ADM CMAP amplitude occurring between 5 and 12 months postinjury. In group A-remain, they found significant recovery of the AHCMAP amplitude. CONCLUSION: . Following SCI, peripheral motor axons below the level of the lesion exhibit severe degeneration. There is partial, although significant, recovery of CMAP during the second half year following SCI. The observed motor axon dysfunction is likely a result of transsynaptic degeneration. The peripheral motor axon dysfunction observed after SCI is of sufficient magnitude that it may affect muscle power and thus contribute to impairment of recovery of functional activities in patients with SCI.

Abstract

OBJECTIVE: . There are indications that perilesional and remote peripheral motor axons may degenerate after spinal cord injury (SCI). The authors investigated the magnitude and dependence on severity of SCI of this degeneration as well as whether motor axons so affected can recover. METHODS: . The function of the peripheral motor axons was investigated by recording compound muscle action potentials (CMAPs) in 345 patients with cervical SCI. CMAP amplitude changes in the abductor digiti minimi (ADM) and abductor hallucis (AH) muscles were investigated in 3 groups with SCIs of differing severity: patients with permanent complete SCI (ASIA Impairment Scale [AIS] A-remain), patients with initially complete SCI converting to incomplete lesion(AISA-convert), and patients with incomplete injury (Incomplete). RESULTS: . Significant decreases in ADM and AH CMAP amplitudes were found in groups A-remain and A-convert. In group A-remain and group A-convert, the authors found a partial, although significant, recovery of ADM CMAP amplitude occurring between 5 and 12 months postinjury. In group A-remain, they found significant recovery of the AHCMAP amplitude. CONCLUSION: . Following SCI, peripheral motor axons below the level of the lesion exhibit severe degeneration. There is partial, although significant, recovery of CMAP during the second half year following SCI. The observed motor axon dysfunction is likely a result of transsynaptic degeneration. The peripheral motor axon dysfunction observed after SCI is of sufficient magnitude that it may affect muscle power and thus contribute to impairment of recovery of functional activities in patients with SCI.

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13 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Balgrist University Hospital, Swiss Spinal Cord Injury Center
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:September 2010
Deposited On:08 Jul 2010 15:22
Last Modified:05 Apr 2016 14:10
Publisher:Sage Publications
ISSN:1545-9683
Publisher DOI:https://doi.org/10.1177/1545968310368534
PubMed ID:20439500

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