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Title: Correlation of response to subthalamic deep brain stimulation in Parkinson's disease patients with striatal dopamine transporter density on 99mtc-TRODAT-1 SPECT. Author: Ghaedian T, Razmkon A, Kalhor L, Ostovan VR, Yousefi O, Rezaei R, Hossein-Tehrani MR, Rakhsha A. Journal: Neurol Res; 2023 Jun; 45(6):505-509. PubMed ID: 36573915. Abstract: BACKGROUND: Deep brain stimulation (DBS) is a surgical approach with electrical stimulation of certain parts of the brain, which reduce Parkinson's disease (PD) symptoms. Since the loss of dopaminergic neurons in the substantia nigra is the main pathophysiology of PD, we aimed to evaluate the association of response to DBS with preoperative dopamine transporter density (DAT) and its postoperative changes in PD patients who underwent the bilateral implantation of the electrodes in the subthalamic nucleus (STN). METHOD: A prospective evaluation of Parkinson's disease patients who underwent STN-DBS for 2 years was done. 99mTc-TRODAT-1 single-photon emission computed tomography (SPECT) scan and assessment of PD using unified Parkinson's disease rating scale (UPDRS) III were performed in both pre- and post-operation states. The correlation of response to DBS after 6 months was assessed with baseline findings and postoperative changes of 99mTc-TRODAT-1 SPECT parameters. RESULTS: Compared to the preoperative state, UPDRS III scores and Levodopa equivalent daily dose (LEDD) were significantly decreased after DBS. However, in 17 patients who underwent both pre-and post-operative 99mTc-TRODAT-1 SPECT, no significant change was seen in any quantitative parameters, including right and left striatal-binding ratio (SBR) as well as striatal asymmetry index (SAI). No significant correlation was also found between the percent of UPDRS III change after DBS and values of preoperative SBRs. The percentage of LEDD reduction also showed no significant correlation with the preoperative state of 99 m-TRODAT-1 SPECT. CONCLUSION: Our results showed that the mechanism of DBS action is not accompanied by short-term compensation of DAT in basal ganglia in severely advanced PD.[Abstract] [Full Text] [Related] [New Search]