Objective: To describe a patient who developed idiopathic delayed-onset edema (IDE) and cognitive decline three days after deep brain stimulation of subthalamic nucleus (STN-DBS).

Background: IDE is a rare, self-limiting complication of DBS procedures. It is defined as a spontaneous edema diffusing along the DBS lead that occurs approximately 72 h after implant, and is not associated with trauma, vascular events or signs of infection. Typical symptoms of IDE are apathy, confusion and seizures, and asymptomatic cases have also been reported.

Method: A 55-year-old man with a 10-year history of Parkinson’s disease was admitted one month after implant, as he developed apathy, memory impairment and apraxia. These symptoms started three days after surgery. DBS had not been activated and the patient was treated with medications only. Past medical history included two episodes of generalized seizures, with last episode sixteen years before.

Results: Cerebrospinal fluid examination revealed slightly increased protein concentration with normal cell count. There was no evidence for viral or bacterial infections. 
Electroencephalogram showed diffuse slowing, with bilateral theta rhythm and sporadic delta waves on the left hemisphere with no evidence of epilepsy. 
Brain magnetic resonance imaging showed bilateral edema and micro-hemorrhages along the DBS electrodes at the level of the left thalamus and supra-adjacent white matter with no associated significant mass effect. The left side was more involved. 
Neuropsychological evaluation showed a decay on tests assessing executive functions (phonemic fluency, Stroop Test and Trial Making Test) and anterograde verbal memory. The scores had worsened compared to a pre-implant assessment. 
Brain metabolic activity was assessed with [18F]-fluorodeoxyglucose positron emission tomography (PET). Brain glucose metabolism was globally decreased, with more involvement of left temporal and parietal lobes.

Conclusion: We describe here a first case of IDE associated with cognitive impairment who underwent a metabolic PET study. IDE-related cognitive decline may not only be related to the involvement of cortical–basal ganglionic circuits along the trajectory, but also by more distant cortical regions. Functional neuroimaging correlated nicely with neuropsychological testing. We are still following the patient with repeated assessments.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/subacute-cognitive-decline-after-dbs-in-a-patient-with-idiopathic-delayed-onset-edema/