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Ineffective subthalamic nucleus stimulation in levodopa-resistant postischemic parkinsonism
P Krack1, P L Dowsey, A L Benabid
1Department of Clinical and Biological Neurosciences, Joseph Fourier University, Grenoble, France. p.krack@neurologie.uni-kiel.de
Neurology
|June 14, 2000
Summary
This study highlights a postischemic parkinsonism case unresponsive to levodopa and subthalamic nucleus (STN) stimulation. Imaging revealed widespread brain lesions, suggesting STN surgery may not suit patients with poor levodopa response or postsynaptic dopaminergic deficits.
Area of Science:
- Neuroscience
- Neurology
- Medical Imaging
Background:
- Parkinsonism can arise from various causes, including ischemia.
- Subthalamic nucleus (STN) deep brain stimulation is a treatment for Parkinson's disease.
- Levodopa is a primary pharmacological treatment for Parkinson's disease.
Observation:
- A patient with postischemic parkinsonism showed no response to levodopa or bilateral STN stimulation.
- MRI revealed bilateral lesions in the substantia nigra, striatum, and pallidum.
- PET scans indicated reduced striatal dopa-decarboxylase activity, D2 receptor binding, and glucose metabolism.
Findings:
- The patient's STN cells exhibited low-frequency activity during perioperative microrecording.
- The observed pattern of neurodegeneration suggests a significant postsynaptic dopaminergic deficit.
Implications:
- Patients with postischemic parkinsonism and poor levodopa response may not benefit from STN surgery.
- Identifying postsynaptic dopaminergic lesions is crucial for predicting treatment outcomes in parkinsonism.
- This case underscores the importance of individualized treatment strategies for complex neurological disorders.