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Closed-Loop Medical Devices Might Reduce Iatrogenic Loss of Autonomous Action Selection

Published online by Cambridge University Press:  22 September 2017

OMAR F.F. ODISH  and
MARTIJN BEUDEL
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Departments and Columns
Information
Cambridge Quarterly of Healthcare Ethics , Volume 26 , Special Issue 4: Clinical Neuroethics , October 2017 , pp. 688 - 690
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Copyright © Cambridge University Press 2017 

We read the article titled “The Effects of Closed-Loop Medical Devices on the Autonomy and Accountability of Persons and Systems” by Kellmeyer et al. Footnote 1 with great interest. The advancing development of brain–computer interfaces (BCIs) indeed necessitates setting up ethical and legal frameworks by experts in the field together with the affected patient populations and their families.

Several examples of BCIs with closed-loop properties are mentioned throughout the article, with a thoughtful consideration of the definition of autonomy, both for the patient and for the device. We write with the purpose of adding an example of an older technology, namely deep brain stimulation (DBS), which recently incorporated closed-loop technology. This was achieved by real-time adaptation of stimulation delivery based on recorded pathological neural activity. Footnote 2,Footnote 3 This closed-loop form of DBS is called adaptive DBS (aDBS). The reason that we want to elaborate on this new technology is that in this case, closed-loop stimulation might increase personal autonomy, instead of decreasing it compared with conventional therapy, which is the case for several current BCI applications mentioned in Kellmeyer’s article.

The potential advantages of this closed-loop interface of aDBS in Parkinson’s disease compared with the conventional continuous, open-loop DBS (cDBS) are multifaceted. It has already been shown that patients receiving aDBS experience fewer speech side effects Footnote 4 and dyskinesias (involuntary movements) Footnote 5 than when receiving cDBS. Furthermore, it is well known that cDBS, as well as dopaminergic medication, can cause behavioral side effects such as disinhibition; Footnote 6,Footnote 7,Footnote 8 however, the potential modulation of this significant side effect with aDBS still needs to be established. It is, therefore, still difficult to ascertain how the closed-loop system of aDBS may affect the autonomy of the patient compared with cDBS. We argue that the development of aDBS might be an example of a closed-loop interaction that would most likely improve patient autonomy, as the stimulation and modification of the neural activity occurs only in those associated with the targeted symptomatology and does not interfere with the physiological neural activity involved in inhibition.

It is thought that the subthalamic nucleus (STN), which is the most common target for DBS in Parkinson’s disease, temporarily increases the threshold for action in cases of conflict, providing extra time for the brain to assess the appropriate decision for a certain situation. Suppression of STN activity, as is the case in cDBS, is expected to lead to “releasing the brake,” thus increasing impulsive behavior in situations of conflict. Footnote 9,Footnote 10,Footnote 11,Footnote 12 Selective suppression of neural activity associated with inhibition of action, as is the case with cDBS in Parkinson’s disease, can modify the patient’s personality and decisionmaking process, and create a feeling of a new identity. Footnote 13

Extensive work on the human (especially Parkinsonian) STN has shown that oscillations in the beta frequency band (13–30 Hz) play an important role in the inhibition of both movements and behavior. Footnote 14,Footnote 15 In line with this, beta oscillations not only correlate with akinesia and rigidity (slowness and stiffness) in the Parkinsonian STN, Footnote 16 but also with the successful suppression of movement during conflict in behavioral paradigms. Footnote 17

To apply DBS in such a way that it both treats bradykinesia and avoids disinhibition, beta-based aDBS appears to be an attractive candidate. One key argument for this is the fact that beta oscillations occur in bursts Footnote 18 : they are only present intermittently. Recent evidence shows that only longer (> 600 ms) beta-bursts were correlated with bradykinesia, Footnote 19 whereas this was not the case for shorter beta-bursts. When analyzing the event-related synchronization in the beta band leading to successful inhibition, the duration of this synchronization is only around 200 ms. Footnote 20,Footnote 21 This leads to the key hypothesis that an aDBS algorithm that selectively targets pathological bursts of beta synchronization longer than 600 ms could be superior to conventional (continuous) stimulation for both motor and nonmotor symptoms.

By alleviating the motor symptoms of Parkinson’s disease while preserving essential cognitive “brakes,” we expect that the closed-loop properties of aDBS will benefit the patient in his or her autonomy as well as preserving his or her identity, although it is necessary to study the effects of aDBS on quality of life and sense of personal autonomy and identity and compare those with the effects of the conventional, open-loop, cDBS.

References

Notes

1. Kellmeyer, P, Cochrane, T, Müller, O, Mitchell, C, Ball, T, Fins, JJ, et al. The effects of closed-loop medical devices on the autonomy and accountability of persons and systems. Cambridge Quarterly of Healthcare Ethics 2016;25(4):623–33.Google Scholar

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3. Piña-Fuentes D, Little S, Oterdoom M, Neal S, Pogosyan A, Tijssen MAJ, et al. Adaptive DBS in a Parkinson’s patient with chronically implanted DBS: A proof of principle. Movement Disorders 2017; doi: 10.1002/mds.26959.

4. Little, S, Tripoliti, E, Beudel, M, Pogosyan, A, Cagnan, H, Herz, D, et al. Adaptive deep brain stimulation for Parkinson’s disease demonstrates reduced speech side effects compared to conventional stimulation in the acute setting. Journal of Neurology, Neurosurgery, and Psychiatry 2016;87(12):1388–9.Google Scholar

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9. See note 7, Witt et al. 2004.

10. See note 8, Frank et al. 2007.

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14. See note 6, Jahanshahi et al. 2000.

15. See note 7, Witt et al. 2004.

16. Beudel, M, Oswal, A, Jha, A, Foltynie, T, Zrinzo, L, Hariz, M, et al. Oscillatory beta power correlates with akinesia-rigidity in the Parkinsonian STN. Movement Disorders 2017;32(1):174–5.CrossRefGoogle Scholar

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20. See note 17, Wessel et al. 2016.

21. Brittain, JS, Watkins, KE, Joundi, RA, Ray, NJ, Holland, P, Green, AL, et al. A role for the subthalamic nucleus in response inhibition during conflict. Journal of Neuroscience 2012;32:13,396–401.Google Scholar