Severe immune rejection leading to refractory peri-electrode edema after DBS: a systematic review and one case report.
Severe immune rejection leading to refractory peri-electrode edema after DBS: a systematic review and one case report.
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The study site has not been established. Author addresses may differ from where the research occurred.
Jinan, CN · Author affiliation
Department of Neurosurgery, Shandong Provincial Hospital, Shandong First Medical University, No. 324, Jingwu Weiqi Road, Huaiyin District, Jinan, 250021, PR China.Location evidence
Tianjin, CN · Author affiliation
Key Laboratory of Post-Neuro Injury, Neuro-Repair and Regeneration in Central Nervous System, Tianjin Neurological Institute, Ministry of Education and Tianjin City, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin, China.Location evidence
Abha, SA · Author affiliation
Department of Physiology, Faculty of Medicine, King Khalid University, Abha, 62529, Saudi Arabia.Location evidence
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Original abstract
Deep brain stimulation (DBS) is a well-established therapy for advanced Parkinson’s disease (PD), yet peri-electrode edema remains a poorly characterized postoperative complication. We present a 51-year-old male with a 9-year history of PD who underwent bilateral subthalamic nucleus (STN)-DBS implantation. Postoperative imaging confirmed accurate electrode placement, and the patient was discharged without immediate complications. However, one week post-surgery, he developed right-sided neck stiffness and spontaneous seizures, followed by progressive right limb weakness and gait impairment. Magnetic resonance imaging (MRI) revealed extensive peri-electrode edema surrounding the right electrode, accompanied by cutaneous erythema and sleep disturbances. Despite aggressive treatment with dexamethasone, antiepileptics, and osmotic diuretics, the edema recurred repeatedly upon dose reduction. Ultimately, the DBS hardware was explanted due to refractory symptoms, with intraoperative findings of inflammatory exudate but no overt infection. This case highlights that peri-electrode edema, though often asymptomatic, may manifest with severe neurological sequelae requiring prolonged intervention. Furthermore, corticosteroid therapy, while effective in acute management, may fail to prevent recurrence in certain patients, necessitating hardware removal. In most cases, the edema resolves without the need for intervention. This case underscores that severe neurological sequelae may arise even after standard management, highlighting the need for individualized therapeutic strategies. Our study provides a comprehensive analysis of the etiological factors, clinical characteristics, and treatment modalities of this condition, offering critical insights to refine its diagnosis and management.