Article
Diffusion tensor imaging (DTI) applied to the medial STN – implications for DBS concerning known side effects and new therapy strategies
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Published: | May 20, 2009 |
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Objective: Neurosurgeons deal with hypomania (4–13%) and depression (20%) in STN DBS for Parkinson disease (PD). However, the anatomical substrate of these effects, typically elicited from medial, inferior and anterior electrode locations, remains unknown. The authors of this study show that an activation of the medial forebrain bundle (MFB), as delimited with DTI, could be the cause of the hypomania.
Methods: Six Patients with advanced PD underwent bilateral STN DBS surgery. Preoperative DTI scans combined with high resolution T1W and T2W sequences, were conducted on a 3T MRI scanner (Philips Healthcare, Best, The Netherlands). In an off-line analysis, the MFB was tracked by using two separate regions of interest in the ventral tegmental area and in the forebrain, including the olfactory tubercle and the accumbens nucleus. After implantation, the DBS electrode positions were determined with CT and integrated in a DTI software environment. (StealthDTI, Medtronic Surgical Navigation, USA)
Results: The medial STN was shown to send tributaries to the MFB as a pathway to the appetitive motivational brain “reward circuitry”. One patient, who had a transient, stimulation - induced acute hypomanic episode at low voltages (2V), showed a direct contact of the active electrode and the limbic STN tributaries to the MFB. In five asymptomatic patients, the active contacts were between 2.9 and 7.5 mm distant from the MFB or its limbic STN tributaries.
Conclusions: The authors hypothesize that STN DBS - induced hypomania represents an activation of the “SEEKING-system” that is part of the so-called hypothalamic “reward circuitry”. MFB anatomy, as rendered with DTI, shows two distinct pathways, possibly related either to reward and/or motivation. Most likely, only the latter is involved in hypomania (i.e., arousal of a “wanting” state). If axonal MFB-arousal can elicit hypomania, then neuronal inhibition (more lateral but inside the medial inferior STN) might trigger depression. These findings may be extrapolated to future investigations on the pathophysiology of psychiatric disorders and might lead into new target areas different from the classical ones for future treatment strategies.