SPECT and PET analysis of subthalamic stimulation in Parkinson's disease: analysis using a manual segmentation.
Identifieur interne : 000A98 ( PubMed/Corpus ); précédent : 000A97; suivant : 000A99SPECT and PET analysis of subthalamic stimulation in Parkinson's disease: analysis using a manual segmentation.
Auteurs : Claire Haegelen ; Daniel García-Lorenzo ; Florence Le Jeune ; Julie Péron ; Bernard Gibaud ; Laurent Riffaud ; Gilles Brassier ; Christian Barillot ; Marc Vérin ; Xavier MorandiSource :
- Journal of neurology [ 1432-1459 ] ; 2010.
English descriptors
- KwdEn :
- Aged, Amygdala (anatomy & histology), Amygdala (diagnostic imaging), Amygdala (physiopathology), Basal Ganglia (anatomy & histology), Basal Ganglia (diagnostic imaging), Basal Ganglia (physiopathology), Brain Mapping (methods), Cognition (physiology), Cognition Disorders (diagnostic imaging), Cognition Disorders (etiology), Cognition Disorders (physiopathology), Deep Brain Stimulation (adverse effects), Emotions (physiology), Female, Hippocampus (anatomy & histology), Hippocampus (diagnostic imaging), Hippocampus (physiopathology), Humans, Image Processing, Computer-Assisted (methods), Limbic System (anatomy & histology), Limbic System (diagnostic imaging), Limbic System (physiopathology), Male, Middle Aged, Mood Disorders (diagnostic imaging), Mood Disorders (etiology), Mood Disorders (physiopathology), Neural Pathways (anatomy & histology), Neural Pathways (diagnostic imaging), Neural Pathways (physiopathology), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Positron-Emission Tomography (methods), Prefrontal Cortex (anatomy & histology), Prefrontal Cortex (diagnostic imaging), Prefrontal Cortex (physiopathology), Subthalamic Nucleus (anatomy & histology), Subthalamic Nucleus (physiology), Tomography, Emission-Computed, Single-Photon (methods).
- MESH :
- adverse effects : Deep Brain Stimulation.
- anatomy & histology : Amygdala, Basal Ganglia, Hippocampus, Limbic System, Neural Pathways, Prefrontal Cortex, Subthalamic Nucleus.
- diagnostic imaging : Amygdala, Basal Ganglia, Cognition Disorders, Hippocampus, Limbic System, Mood Disorders, Neural Pathways, Prefrontal Cortex.
- etiology : Cognition Disorders, Mood Disorders.
- methods : Brain Mapping, Image Processing, Computer-Assisted, Positron-Emission Tomography, Tomography, Emission-Computed, Single-Photon.
- physiology : Cognition, Emotions, Subthalamic Nucleus.
- physiopathology : Amygdala, Basal Ganglia, Cognition Disorders, Hippocampus, Limbic System, Mood Disorders, Neural Pathways, Parkinson Disease, Prefrontal Cortex.
- therapy : Parkinson Disease.
- Aged, Female, Humans, Male, Middle Aged.
Abstract
The subthalamic nucleus (STN) has become an effective target of deep-brain stimulation (DBS) in severely disabled patients with advanced Parkinson's disease (PD). Clinical studies have reported DBS-induced adverse effects on cognitive functions, mood, emotion and behavior. STN DBS seems to interfere with the limbic functions of the basal ganglia, but the limbic effects of STN DBS are controversial. We measured prospectively resting regional cerebral metabolism (rCMb) with 18-fluorodeoxyglucose and PET, and resting regional cerebral blood flow (rCBF) with HMPAO and SPECT in six patients with Parkinson's disease. We compared PET and SPECT 1 month before and 3 months after STN DBS. On cerebral MRI, 13 regions of interest (ROI) were manually delineated slice by slice in frontal and limbic lobes. We obtained mean rCBF and rCMb values for each ROI and the whole brain. We normalized rCBF and rCMB values to ones for the whole brain volume, which we compared before and following STN DBS. No significant difference emerged in the SPECT analysis. PET analysis revealed a significant decrease in rCMb following STN DBS in the superior frontal gyri and left and right dorsolateral prefrontal cortex (p < 0.05). A non-significant decrease in rCMb in the left anterior cingulate gyrus appeared following STN DBS (p = 0.075). Our prospective SPECT and PET study revealed significantly decreased glucose metabolism of the two superior frontal gyri without any attendant perfusion changes following STN DBS. These results suggest that STN DBS may change medial prefrontal function and therefore the integration of limbic information, either by disrupting emotional processes within the STN, or by hampering the normal function of a limbic circuit.
DOI: 10.1007/s00415-009-5327-8
PubMed: 19774437
Links to Exploration step
pubmed:19774437Le document en format XML
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<term>Basal Ganglia (anatomy & histology)</term>
<term>Basal Ganglia (diagnostic imaging)</term>
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<front><div type="abstract" xml:lang="en">The subthalamic nucleus (STN) has become an effective target of deep-brain stimulation (DBS) in severely disabled patients with advanced Parkinson's disease (PD). Clinical studies have reported DBS-induced adverse effects on cognitive functions, mood, emotion and behavior. STN DBS seems to interfere with the limbic functions of the basal ganglia, but the limbic effects of STN DBS are controversial. We measured prospectively resting regional cerebral metabolism (rCMb) with 18-fluorodeoxyglucose and PET, and resting regional cerebral blood flow (rCBF) with HMPAO and SPECT in six patients with Parkinson's disease. We compared PET and SPECT 1 month before and 3 months after STN DBS. On cerebral MRI, 13 regions of interest (ROI) were manually delineated slice by slice in frontal and limbic lobes. We obtained mean rCBF and rCMb values for each ROI and the whole brain. We normalized rCBF and rCMB values to ones for the whole brain volume, which we compared before and following STN DBS. No significant difference emerged in the SPECT analysis. PET analysis revealed a significant decrease in rCMb following STN DBS in the superior frontal gyri and left and right dorsolateral prefrontal cortex (p < 0.05). A non-significant decrease in rCMb in the left anterior cingulate gyrus appeared following STN DBS (p = 0.075). Our prospective SPECT and PET study revealed significantly decreased glucose metabolism of the two superior frontal gyri without any attendant perfusion changes following STN DBS. These results suggest that STN DBS may change medial prefrontal function and therefore the integration of limbic information, either by disrupting emotional processes within the STN, or by hampering the normal function of a limbic circuit.</div>
</front>
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<Abstract><AbstractText>The subthalamic nucleus (STN) has become an effective target of deep-brain stimulation (DBS) in severely disabled patients with advanced Parkinson's disease (PD). Clinical studies have reported DBS-induced adverse effects on cognitive functions, mood, emotion and behavior. STN DBS seems to interfere with the limbic functions of the basal ganglia, but the limbic effects of STN DBS are controversial. We measured prospectively resting regional cerebral metabolism (rCMb) with 18-fluorodeoxyglucose and PET, and resting regional cerebral blood flow (rCBF) with HMPAO and SPECT in six patients with Parkinson's disease. We compared PET and SPECT 1 month before and 3 months after STN DBS. On cerebral MRI, 13 regions of interest (ROI) were manually delineated slice by slice in frontal and limbic lobes. We obtained mean rCBF and rCMb values for each ROI and the whole brain. We normalized rCBF and rCMB values to ones for the whole brain volume, which we compared before and following STN DBS. No significant difference emerged in the SPECT analysis. PET analysis revealed a significant decrease in rCMb following STN DBS in the superior frontal gyri and left and right dorsolateral prefrontal cortex (p < 0.05). A non-significant decrease in rCMb in the left anterior cingulate gyrus appeared following STN DBS (p = 0.075). Our prospective SPECT and PET study revealed significantly decreased glucose metabolism of the two superior frontal gyri without any attendant perfusion changes following STN DBS. These results suggest that STN DBS may change medial prefrontal function and therefore the integration of limbic information, either by disrupting emotional processes within the STN, or by hampering the normal function of a limbic circuit.</AbstractText>
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