Abstract
Deep brain stimulation (DBS) provides therapeutic benefit for several neuropathologies, including Parkinson disease (PD), epilepsy, chronic pain, and depression. Despite well-established clinical efficacy, the mechanism of DBS remains poorly understood. In this review, we begin by summarizing the current understanding of the DBS mechanism. Using this knowledge as a framework, we then explore a specific hypothesis regarding DBS of the subthalamic nucleus (STN) for the treatment of PD. This hypothesis states that therapeutic benefit is provided, at least in part, by activation of surviving nigrostriatal dopaminergic neurons, subsequent striatal dopamine release, and resumption of striatal target cell control by dopamine. While highly controversial, we present preliminary data that are consistent with specific predications testing this hypothesis. We additionally propose that developing new technologies (e.g., human electrometer and closed-loop smart devices) for monitoring dopaminergic neurotransmission during STN DBS will further advance this treatment approach.
Original language | English (US) |
---|---|
Pages (from-to) | 85-103 |
Number of pages | 19 |
Journal | Neuromodulation |
Volume | 12 |
Issue number | 2 |
DOIs | |
State | Published - Apr 2009 |
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Keywords
- Deep brain stimulation
- Parkinson disease
- Subthalamic nucleus
- Voltammetry
- Wireless integrated circuit
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine
- Neurology
- Clinical Neurology
Cite this
Evolution of deep brain stimulation : Human electrometer and smart devices supporting the next generation of therapy. / Lee, Kendall H; Blaha, Charles D.; Garris, Paul A.; Mohseni, Pedram; Horne, April E.; Bennet, Kevin E.; Agnesi, Filippo; Bledsoe, Jonathan M.; Lester, Deranda B.; Kimble, Chris; Min, Hoon Ki; Kim, Young Bo; Cho, Zang Hee.
In: Neuromodulation, Vol. 12, No. 2, 04.2009, p. 85-103.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Evolution of deep brain stimulation
T2 - Human electrometer and smart devices supporting the next generation of therapy
AU - Lee, Kendall H
AU - Blaha, Charles D.
AU - Garris, Paul A.
AU - Mohseni, Pedram
AU - Horne, April E.
AU - Bennet, Kevin E.
AU - Agnesi, Filippo
AU - Bledsoe, Jonathan M.
AU - Lester, Deranda B.
AU - Kimble, Chris
AU - Min, Hoon Ki
AU - Kim, Young Bo
AU - Cho, Zang Hee
PY - 2009/4
Y1 - 2009/4
N2 - Deep brain stimulation (DBS) provides therapeutic benefit for several neuropathologies, including Parkinson disease (PD), epilepsy, chronic pain, and depression. Despite well-established clinical efficacy, the mechanism of DBS remains poorly understood. In this review, we begin by summarizing the current understanding of the DBS mechanism. Using this knowledge as a framework, we then explore a specific hypothesis regarding DBS of the subthalamic nucleus (STN) for the treatment of PD. This hypothesis states that therapeutic benefit is provided, at least in part, by activation of surviving nigrostriatal dopaminergic neurons, subsequent striatal dopamine release, and resumption of striatal target cell control by dopamine. While highly controversial, we present preliminary data that are consistent with specific predications testing this hypothesis. We additionally propose that developing new technologies (e.g., human electrometer and closed-loop smart devices) for monitoring dopaminergic neurotransmission during STN DBS will further advance this treatment approach.
AB - Deep brain stimulation (DBS) provides therapeutic benefit for several neuropathologies, including Parkinson disease (PD), epilepsy, chronic pain, and depression. Despite well-established clinical efficacy, the mechanism of DBS remains poorly understood. In this review, we begin by summarizing the current understanding of the DBS mechanism. Using this knowledge as a framework, we then explore a specific hypothesis regarding DBS of the subthalamic nucleus (STN) for the treatment of PD. This hypothesis states that therapeutic benefit is provided, at least in part, by activation of surviving nigrostriatal dopaminergic neurons, subsequent striatal dopamine release, and resumption of striatal target cell control by dopamine. While highly controversial, we present preliminary data that are consistent with specific predications testing this hypothesis. We additionally propose that developing new technologies (e.g., human electrometer and closed-loop smart devices) for monitoring dopaminergic neurotransmission during STN DBS will further advance this treatment approach.
KW - Deep brain stimulation
KW - Parkinson disease
KW - Subthalamic nucleus
KW - Voltammetry
KW - Wireless integrated circuit
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U2 - 10.1111/j.1525-1403.2009.00199.x
DO - 10.1111/j.1525-1403.2009.00199.x
M3 - Article
AN - SCOPUS:65349085578
VL - 12
SP - 85
EP - 103
JO - Neuromodulation
JF - Neuromodulation
SN - 1094-7159
IS - 2
ER -