Martin Kronenbuerger1,2, Kay Wilhelm Nolte3, Volker Arnd Coenen4, Jean-Marc Burgunder5, Joachim K Krauss6, Joachim Weis3. 1. Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA. 2. Department of Neurology, RWTH Aachen University Hospital, Aachen, Germany. 3. Institute of Neuropathology, RWTH Aachen University Hospital, Aachen, Germany. 4. Department of Stereotactic and Functional Neurosurgery, Freiburg University Medical Center, Freiburg, Germany. 5. Department of Neurology, University of Berne, Inselspital, Berne, Switzerland. 6. Department of Neurosurgery, Medical School Hannover (MHH), Hannover, Germany.
Abstract
BACKGROUND: Previous studies on human brain tissue alterations caused by deep brain stimulation described glial and reactive inflammatory changes. In the current pathoanatomical study, we extended the analysis to signs of axonal changes and the influence of concomitant disease. METHODS: Brains of 10 patients with Parkinson's disease or essential tremor and a total of 18 electrodes were systematically examined up to 7.5 y after surgery. RESULTS: In general, tissue that had long-term contact with the electrode material exhibited astrogliosis in all, T-lymphocytes in 93%, and multinucleated giant cells in 68% of patients. Immunohistochemistry showed an increase in amyloid precursor protein immunoreactive axonal swellings in the brain at the electrically active parts of the electrodes. Patients who died of septicemia showed a more severe astrogliosis and giant cell reaction than patients who died of cardiovascular events. Parkinson's disease or essential tremor did not differentially produce histopathological changes around the electrodes. CONCLUSION: Long-term electrical stimulation by deep brain stimulation causes minor axonal changes. The cause of death, but not the underlying neurological disease, affects the histopathological changes around the electrode. The findings need to be reproduced by examining larger patient subgroups.
BACKGROUND: Previous studies on human brain tissue alterations caused by deep brain stimulation described glial and reactive inflammatory changes. In the current pathoanatomical study, we extended the analysis to signs of axonal changes and the influence of concomitant disease. METHODS: Brains of 10 patients with Parkinson's disease or essential tremor and a total of 18 electrodes were systematically examined up to 7.5 y after surgery. RESULTS: In general, tissue that had long-term contact with the electrode material exhibited astrogliosis in all, T-lymphocytes in 93%, and multinucleated giant cells in 68% of patients. Immunohistochemistry showed an increase in amyloid precursor protein immunoreactive axonal swellings in the brain at the electrically active parts of the electrodes. Patients who died of septicemia showed a more severe astrogliosis and giant cell reaction than patients who died of cardiovascular events. Parkinson's disease or essential tremor did not differentially produce histopathological changes around the electrodes. CONCLUSION: Long-term electrical stimulation by deep brain stimulation causes minor axonal changes. The cause of death, but not the underlying neurological disease, affects the histopathological changes around the electrode. The findings need to be reproduced by examining larger patient subgroups.
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