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. 2025 Mar 6;13(3):e70221.
doi: 10.1002/ccr3.70221. eCollection 2025 Mar.

An Unusual Presentation of Peri-Lead Edema Following Deep Brain Stimulation for Parkinson's Disease: A Case Report and Review of the Literature

Affiliations

An Unusual Presentation of Peri-Lead Edema Following Deep Brain Stimulation for Parkinson's Disease: A Case Report and Review of the Literature

V S Witzig et al. Clin Case Rep. .

Abstract

Peri-lead edema (PLE) after deep brain stimulation may mimic brain infection on magnetic resonance imaging (MRI). We present a case of symptomatic PLE with annular contrast enhancement on MRI suggestive of an infectious cause. We show that careful clinical evaluation and laboratory testing, in addition to neuroimaging, are essential to guide treatment and to avoid unnecessary interventions in PLE cases with a favorable spontaneous course.

Keywords: Parkinson's disease; deep brain stimulation; movement disorders; neuromodulation; peri‐lead edema.

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Conflict of interest statement

M.W. is working as a consultant for Stryker Neurovascular. M.W. has been working as a consultant for Kaneka Pharmaceuticals and Medtronic (both inactive). M.W. has received reimbursement for lectures or travel support from Bracco Imaging, Medtronic, Siemens Healthcare, and Stryker Neurovascular. M.W. has received grants for research projects or educational exhibits from ab medica, Acandis, Bayer, Bracco Imaging, Cerenovus, Codman Neurovascular, Dahlhausen, Kaneka Pharmaceuticals, Medtronic, Mentice AB, Microvention, Phenox, Siemens Healthcare, and Stryker Neurovascular. J.B.S. is working in the advisory board of Forward Pharma, MSD, Lundbeck, Biogen, Eisai, Novo Nordisk, Roche, Reata, and Lilly. J.B.S. has received reimbursement for lectures from Merz, Teva, Bayer, UCB, Lilly, Boehringer, GSK, Bial, Novartis, Biogen, and Eisai. J.B.S. has received grants for research projects from Biogen, Eisai, and Lilly. F.H. received travel and conference fees from Bial, Desitin, Abbott, Zambon, and Abbvie. V.S.W. received travel and conference fees from Medtronic. The other authors declare no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Exemplary radiological findings of longitudinal CT scans. (A) CT on postoperative day two showed bifrontal hypodensities around the electrodes. (B) CT on postoperative day 4 revealed progressive edema (marked with arrows).
FIGURE 2
FIGURE 2
Longitudinal evaluation of brain MRI. (A) MRI pre surgery showing several microvascular white matter lesions. (B) Extensive edema as reflected by hyperintensities on T2‐weighted fluid‐attenuated inversion recovery (FLAIR) MRI on day 6 post‐surgery along the electrodes' trajectories, pronounced on the right side (marked with arrows). (C) Bilateral cortical annular contrast enhancement (CE) on both sides, marked on the right side (marked with arrows). (D) Diffusion weighted imaging (DWI) revealed no signal restriction in the area of annular CE (limited accessibility due to metal artifacts) but suggested right thalamic infarction (marked with arrow) with corresponding signal on the ADC‐map (E). (F) Follow‐up MRI at week 10 postsurgery showed near complete remission of edema on FLAIR imaging with complete remission of CE on T1‐weighted MRI (G). There was no sign of (chronic) ischemic infarction in the right thalamus (H, I).

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