Neuromagnetic Stimulation at Selected Spinal Levels Can Significantly Influence Endocrine Function

Paul J. Maccabee, R. Atluri, D. Jagoo, J.A. Willer, A.B. Ahad, A.Z. Szabo, H.G. Durkin, M. Nowakowski, M.A. Banerji, P.M. Gootman, V.E. Amassian, R.Q. Cracco, H.E. Lebovitz
Wednesday April 16 7:30 am / Exhibit Hall A

It was hypothesized that neuromagnetic stimuli delivered by a large twin magnetic coil with the junction held horizontally over specific thoraco-lumbar spinal levels might selectively excite autonomic fibers innervating specific endocrine organs.

Earlier work showed that a large twin magnetic coil can excite the cauda equina (Maccabee et al, Electroenceph. clin. Neurophys. 1996, 101, 153-166).

Four adult male volunteers were studied in the lateral decubitus position after 30 minutes of supine posture (NPO for at least 8 hrs). 50 maximal or near maximal stimuli were given (6/minute) with the MC junction held horizontally between T8 and T11 (3 subjects) or vertically centered over the same region (1 subject). Venous blood was sampled from an indwelling catheter before, during, and after stimulation over 6 hrs; measurements were made of insulin, cortisol, glucose, glucagon, norepinephrine, epinephrine, dopamine, aldosterone, testosterone, CBC, PT, PTT, lymphocyte subsets, cytokines, and SMA-18. Additional samples were also obtained daily up to four days before and eleven days after stimulation.

In all subjects the major consistent finding was a decline from as little as 18% to more than 54% in serum insulin level compared to baseline between one and five minutes following stimulation onset. The greatest initial decline in insulin was observed in the subject who was insulin resistant with abnormally elevated insulin levels ("pre-diabetic"). In all subjects, serum glucose levels remained steady throughout. In addition, serum cortisol was significantly reduced compared to baseline (maximum 34%); the reduction was most prominent in three subjects at one hour post-stimulation onset. Other measures showed less consistent changes.

Further analysis is needed to determine if the above findings reflect direct stimulation of visceral afferents, pre-ganglionic sympathetic efferents, splanchnic nerves, or target organs directly. Activation of somatic musculature may also indirectly contribute. This approach may allow us to elucidate mechanisms of inhibition of insulin secretion during severe hyperglycemia in diabetes.

Sponsored by: Department of Neurology.

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