Serotonergic neuronal atrophy with synaptic inactivation, not axonal degeneration, are the main hallmarks of multiple sclerosis.
The neurological manifestations of multiple sclerosis (MS) have been considered to result from demyelination of axons with relative preservation of axonal integrity. This concept has been challenged recently by a landmark pathological study, published in the New England Journal of Medicine, which has demonstrated that axonal degeneration is also present. The authors of the study hypothesized that axonal degeneration is the pathological correlate of the irreversible neurological impairment in this disease. However, this hypothesis cannot be reconciled with the clinical results obtained with transcranial applications of AC pulsed electromagnetic fields (EMFs) of picotesla flux density which have shown rapid and sustained improvement of symptoms including normalization of evoked potential responses in patients with chronic progressive or secondary progressive MS without demyelinated areas first undergoing remyelination or transected axons undergoing regeneration. Biochemical studies have shown that MS patients are serotonergically depleted with the extent of cerebral depletion correlating with the degree of motor disability and a chronic progressive course. It is believed that progressive serotonergic neuronal atrophy with synaptic inactivation, not axonal degeneration, are the hallmarks of the disease and that administration of AC pulsed magnetic fields improves symptoms of MS partly through reactivation of serotonergic neurons and amplification of synaptic serotonergic transmission.
Sandyk
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Department of Neuroscience at the Institute for Biomedical Engineering and Rehabilitation Services of Touro College, Dix Hills, NY 11746, USA.
D001284:Atrophy; D001369:Axons / Q000473:pathology*; D001921:Brain / Q000473:pathology; D006801:Humans; D009103:Multiple Sclerosis / Q000473:pathology*; D009410:Nerve Degeneration / Q000473:pathology; D009474:Neurons / Q000473:pathology* / Q000648:ultrastructure; D012701:Serotonin / Q000502:physiology*; D013569:Synapses / Q000502:physiology*
D012701:Serotonin