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Motor Pathway Analysis in HAM/TSP Using Magnetic Stimulation and F-waves

Published online by Cambridge University Press:  18 September 2015

Ronald E. Young*
Affiliation:
Departments of Basic Medical Sciences, Faculty of Medical Sciences, University of the West Indies, Mona, Jamaica
Owen C. Morgan
Affiliation:
Medicine, Faculty of Medical Sciences, University of the West Indies, Mona, Jamaica
Allan Forster
Affiliation:
Neurophysiology, Dundee Royal Infirmary, Dundee, Scotland
*
Departments of Basic Medical Sciences, University of the West Indies, Mona,Kingston 7, Jamaica, West Indies.
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Abstract:

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Background:

Tropical Spastic Paraparesis/HTLV-I Associated Myelopathy (HAM/TSP) is a chronic, progressive myelopathy endemic to the Caribbean. In HAM/TSP, peripheral motor pathways have been assessed using electromyography and nerve conduction studies; central motor pathways have been assessed to a limited extent using electrocortical stimulation. We used magnetic cortical stimulation (a painless alternative to electrocortical stimulation) and F-wave analysis to study conduction in the central and peripheral motor pathways in 18 HTLV-I seropositive, Jamaican TSP patients (ages 29- 70 years; duration of symptoms 3-20 years) and 22 normal controls.

Methods:

Magnetic cortical stimulation was effected using a 9 cm diameter undamped MES10 coil. F-waves and M-responses were elicited by electrical stimulation of the ulnar nerve at the wrist, and deep peroneal stimulation at the knee. Stimulation and recording of response latencies in abductor digitii minimi (ADM) and tibialis anterior (TA) were carried out using a Cadwell Excel system.

Results:

With cortical stimulation, response latencies (TMCTs) to ADM and TA were prolonged in the patients relative to controls. F-wave and M-response latencies were unaffected, suggesting no peripheral pathology. Latency (CMCT) between cortex and lumbar cord was significantly prolonged; that between cortex and C7/T1, also, but less markedly (P < 0.0005). Amplitudes of cortically evoked responses were significantly reduced only in the lower limbs (TA). CMCT increased as the disease progressed from mild to moderate, thereafter remaining largely unchanged.

Conclusions:

Meta-analysis of interlaboratory control data revealed no significant differences in TMCTs between our controls and others studied using similar techniques. The observations are consistent with pathology affecting mainly the thoracolumbar cord in HAM/TSP.

Type
Original Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1998

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