Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 58, Num. 5, 2010, pp. 796-797

Neurology India, Vol. 58, No. 5, September-October, 2010, pp. 796-797

Letter to Editor

Magnetic augmented translumbosacral stimulation coil stimulation method for accurate evaluation of corticospinal tract function in peripheral neuropathy

Hideyuki Matsumoto¹, Yuichiro Shirota¹, Yoshikazu Ugawa²

¹ Department of Neurology, Division of Neuroscience, Graduate School of Medicine, The University of Tokyo, Japan
² Department of Neurology, School of Medicine, Fukushima Medical University, Japan

Correspondence Address:
Hideyuki Matsumoto
Department of Neurology, Division of Neuroscience, Graduate School of Medicine, The University of Tokyo
Japan
hideyukimatsumoto.jp@gmail.com

Date of Acceptance: 27-Jul-2010

Code Number: ni10223

PMID: 21045521

DOI: 10.4103/0028-3886.72183

Sir,

The limitation of magnetic stimulation is that the prolongation of the central motor conduction time (CMCT) does not exactly indicate the involvement of the corticospinal tract when the spinal nerves are involved, because magnetic stimulation over the spinal enlargements activates the spinal nerves at the neuro-foramina level. ^[1] Especially for leg muscles, the conduction delay of long spinal nerves (i.e., cauda equina) readily contributes to CMCT prolongation. Recently, we have developed a novel method to activate the most proximal cauda equina around the conus medullaris using a magnetic augmented translumbosacral stimulation (MATS) coil [Figure - 1]. ^[2] We have also reported that the conduction time from the motor cortex to the conus medullaris (cortico-conus motor conduction time, CCCT) can be assessed using the MATS coil in healthy subjects. ^[3] Here, we demonstrate that the CCCT is hardly affected even when the nerve conduction of peripheral nerves is severely delayed.

The patient was a 28-year-old man who presented with muscle weakness, sensory disturbance and areflexia. He had no complaint or symptom related to corticospinal tract. He has been diagnosed as a case of Charcot-Marie-Tooth (CMT) disease type 1 after gene analysis, a mutation of myelin protein zero. Nerve conduction studies showed severe slowing of conduction (<10 m/s) in the upper and lower extremities. A MATS coil stimulation study was performed to measure CCCT [Figure - 2]. Motor-evoked potentials were recorded from the right biceps femoris muscle. This proximal muscle was selected because it was intact, compared to the distal muscles with severe muscular atrophy. Transcranial magnetic stimulation was performed during voluntary contraction of the target muscle. The cortical latency was severely prolonged [133.2 ms; normal value is 21.8±1.0 ms (mean±SD, the data of age- and body height-matched 10 normal subjects)]. Subsequent L1 level MATS coil stimulation performed during relaxation showed that the L1 level latency was also severely prolonged (119.8 ms; normal value, 8.9±0.8 ms). In contrast, the CCCT was within normal limits (13.4 ms; normal value, 12.9±1.1 ms).

In CMT disease, peripheral motor conduction is uniformly involved both proximally and distall, ^[4] although the central motor conduction is intact. Indeed, the CCCT was normal. Therefore, we consider that the CCCT obtained using the MATS coil stimulation method is a useful parameter to evaluate the accurate corticospinal tract function, even in patients with severe peripheral neuropathy. In earlier reports of hereditary neuropathies, a possibility of involvement of central pathways has been raised, ^[5] which could have been caused by a faulty technique of CMCT measurement. Furthermore, methods to measure CMCT using F-waves or tendon reflex latency (T-response) also are unreliable in cases of proximal nerve conduction delay. For reliability of the direct activation of the most proximal cauda equina, we propose that the central motor conduction be evaluated using the MATS coil stimulation method in patients with peripheral neuropathy.

Acknowledgments

We are grateful to Drs. Ritsuko Hanajima, Masashi Hamada and Yasuo Terao (Department of Neurology, The University of Tokyo, Japan) for advice in this investigation.

References

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