One of the greatest challenges confronting the neurotechnology industry in the years ahead is uncovering the mechanisms by which neuromodulation therapies such as DBS exert their effect. This is not only important for the maturation of the clinical modality, but also for the growth of new products, since regulators and insurers are increasingly interested in therapies that are well understood.
Mechanisms of action were at the forefront of the recent meeting of the North American Neuromodulation Society [see conference report, p7]. Readers of this publication have benefited for several years from NBR senior technical editor Warren Grill’s descriptions of new research findings and their potential commercial implications. But Grill’s own work, in particular his concept of the “informational lesion,” stands to transform the field in a significant way, in this editor’s opinion.
Grill’s ideas about maintaining fidelity of stimulation patterns for several synaptic levels downstream of their origin provide a tidy conceptual framework for understanding how DBS achieves its therapeutic effect. More important, the model goes a long way toward elucidating neurophysiological processes in the normally functioning brain and the etiology of different disease states. Just as previous medical advances have been prompted by the discovery of a nasty virus or bacterium or molecule, the “toxin” in neurological disorders ranging from tremor to depression may prove to be faulty signals such as burst activity emanating from neural centers somewhere within a circuit that controls a particular motor behavior, emotional affect, or cognitive task. Locating this informational toxin, decoding its aberrant signal patterns, and treating the “lesion” with therapeutic doses of electrical current, optical illumination, or neurochemical transmitters applied at the appropriate juncture within a circuit may be how medicine is practiced in the future, at least as it relates to neurological disorders.
These tools and processes highlight one more advantage of DBS over surgical interventions, beyond the efficacy superiority we discuss on page 1 of this issue. Indeed, the informational lesion concept points up the folly of surgical ablation of a neural center that may contribute signals to multiple neural circuits, only one of which is pathological. Worse, surgical ablation could conceivably target an innocent neural center that is faithfully transcribing a pathological signal that originated upstream. There may be differences among individuals with the same disorder as to the optimal locus of informational intervention or their may be different “strains” of viral signals that produce slightly different symptoms.
We salute the neural engineers, neurosurgeons, and other specialists pursuing these informational pathogens and building a new generation of neurological therapies.
Editor and Publisher