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Published on: May 31, 2016
Medial forebrain bundle stimulation as a pathophysiological mechanism for hypomania in subthalamic nucleus deep brain
Volker A Coenen1, Christopher R Honey, Trevor Hurwitz
1Surgical Center for Movement Disorders, University of British Columbia, Vancouver, BC, Canada. vacoenen@aol.com
Objective:
Hypomania accounts for approximately 4% to 13% of psychotropic adverse events during subthalamic nucleus (STN) deep brain stimulation (DBS) for Parkinson's disease. Diffusion of current into the inferior and medial "limbic" STN is often reported to be the cause. We suggest a different explanation, in which the coactivation of the medial forebrain bundle (MFB), outside the STN, leads to hypomania during STN DBS.
Methods:
Six patients with advanced Parkinson's disease (age, 54 +/- 11 years) underwent bilateral STN DBS surgery. Preoperative diffusion tensor imaging scans for fiber tracking of the MFB were conducted on a 3T magnetic resonance imaging scanner. After implantation, the electrode positions were determined with computed tomography and integrated in a diffusion tensor imaging software environment.
Results:
The medial STN was shown to send tributaries to the MFB using it as a pathway to connect to the reward circuitry. One patient, who had a transient, stimulation-induced acute hypomanic episode, showed a direct contact between 1 active electrode contact and these putative limbic STN tributaries to the MFB unilaterally on the left. In 5 asymptomatic patients, the active contacts were between 2.9 and 7.5 mm distant from the MFB or its limbic STN tributaries.
Conclusion:
We hypothesize that STN DBS-induced reversible acute hypomania might be elicited by inadvertent and unilateral coactivation of putative limbic STN tributaries to the MFB. These findings may provide insight into the neural pathways of hypomania and may facilitate future investigations of the pathophysiology of mood disorders.
Insights
Subthalamic nucleus deep brain stimulation (STN DBS) for Parkinson's disease may cause hypomania by activating the medial forebrain bundle (MFB). This study suggests MFB coactivation, not just STN diffusion, triggers hypomanic episodes.
Area of Science:
- Neuroscience
- Neurosurgery
- Psychiatry
Background:
- Hypomania is a significant adverse event in subthalamic nucleus deep brain stimulation (STN DBS) for Parkinson's disease.
- Current diffusion into the limbic STN is the presumed cause of hypomania.
- An alternative hypothesis involves the medial forebrain bundle (MFB).
Purpose of the Study:
- To investigate the hypothesis that medial forebrain bundle (MFB) coactivation, rather than solely STN diffusion, causes hypomania during STN DBS.
- To explore the neural pathways underlying hypomania in Parkinson's disease patients undergoing STN DBS.
Main Methods:
- Bilateral STN DBS was performed on six Parkinson's disease patients.
- Preoperative diffusion tensor imaging (DTI) fiber tracking identified the MFB.
- Postoperative CT scans localized electrode positions within a DTI environment.
Main Results:
- The medial STN connects to the MFB, which links to reward circuitry.
- One patient experiencing hypomania had direct contact between an active electrode and limbic STN-MFB tributaries.
- Asymptomatic patients had active contacts millimeters away from these pathways.
Conclusions:
- STN DBS-induced hypomania may result from inadvertent, unilateral coactivation of limbic STN tributaries to the MFB.
- These findings offer insights into the neural basis of hypomania.
- This research may guide future studies on mood disorder pathophysiology.
