Voxel-based comparison of regional cerebral glucose metabolism between PSP and corticobasal degeneration

Hosaka, Kayo; Ishii, Kazunari; Sakamoto, Setsu; Mori, Tetsuya; Sasaki, Masahiro; Hirono, Nobutsugu; Mori, Etsuro

doi:10.1016/s0022-510x(02)00102-8

Cited by 85 publications

(48 citation statements)

References 16 publications

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“…Likewise, imaging results in patients with clinically diagnosed PSP and CBD may be very similar. In direct comparison of clinically defined patient groups, PSP patients showed a lower metabolism in the midbrain, thalamus, and cingulate gyrus, whereas CBD patients revealed a more pronounced and asymmetric hypometabolism in the parietal and sensorimotor cortex and striatum (51)(52)(53)(54). According to recent studies with support by postmortem data, parietal involvement and the asymmetry of the aforementioned frontoparietal hypometabolism appear to be most characteristic of CBD (45,55).…”

Section: Disease-specific Patterns Of Regional Glucose Metabolismmentioning

confidence: 90%

¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

et al. 2017

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Learning Objectives: On successful completion of this activity, participants should be able to (1) describe the clinical demand and rationale for differential diagnosis in parkinsonism, (2) recognize and differentiate the disease-specific patterns of regional glucose metabolism associated with Parkinson disease and the different atypical parkinsonian syndromes, and (3) identify regional metabolic changes that predict cognitive decline in Parkinson disease.Financial Disclosure: Dr. Meyer receives support from GE and Piramal for a research study outside the present topic. The authors of this article have indicated no other relevant relationships that could be perceived as a real or apparent conflict of interest. CME Credit: SNMMI is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to sponsor continuing education for physicians. SNMMI designates each JNM continuing education article for a maximum of 2.0 AMA PRA category 1 credits. Physicians should claim only credit commensurate with the extent of their participation in the activity. For CE credit, SAM, and other credit types, participants can access this activity through the SNMMI website (http://www.snmmilearningcenter.org) through December 2020.Accurate differential diagnosis of parkinsonism is of paramount therapeutic and prognostic importance. In addition, with the development of invasive therapies and novel disease-specific therapies, strategies for patient enrichment in trial populations are of growing importance. Imaging disease-specific patterns of regional glucose metabolism with PET and 18 F-FDG allows for a highly accurate distinction between Parkinson disease (PD) and atypical parkinsonian syndromes, including multiple-system atrophy, progressive supranuclear palsy, and corticobasal degeneration. On the basis of a preliminary metaanalysis of currently available studies with inclusion of multiple disease groups, we estimated that the diagnostic sensitivity and specificity for visual PET readings supported by voxel-based statistical analyses for diagnosis of atypical parkinsonian syndromes are 91.4% and 90.6%, respectively. The diagnostic specificity of 18 F-FDG PET for diagnosing multiple-system atrophy, progressive supranuclear palsy, and corticobasal degeneration was consistently shown to be high (.90%), whereas sensitivity was more variable (.75%). It is increasingly acknowledged that cognitive impairment represents a major challenge in PD, with mild cognitive impairment being a prodromal stage of PD with dementia (PDD). In line with clinical and neuropsychologic studies, recent PET studies demonstrated that posterior cortical dysfunction in nondemented PD patients precedes cognitive decline and the development of PDD by several years. Taken together, the current literature underscores the utility of 18 F-FDG PET for diagnostic evaluation of parkinsonism and the promising role of 18 F-FDG PET for assessment and risk stratification of cognitive impairment in PD.

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Section: Disease-specific Patterns Of Regional Glucose Metabolismmentioning

confidence: 90%

¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

et al. 2017

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“…This suggests that apathy is the consequence of a "prefrontal-like" syndrome due to lesions mostly affecting the basal ganglia. In consequence, the massive hypometabolism of the anterior portion of the frontal lobes [27,33,59], in particular in the superior lateral and medial PFC [14, 46,59] that correlates with the behavioral syndrome, can be interpreted as the result of a deafferentation prefrontal syndrome due to basal ganglia lesions.…”

Section: Apathy In Parkinson's Diseasementioning

confidence: 99%

Apathy and the basal ganglia

Lévy

Czernecki

2006

J Neurol

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We should like to emphasize the following points: 1. Apathy is defined here as a quantified and observable behavioral syndrome consisting in a quantitative reduction of voluntary (or goal-directed) behaviors; 2. Therefore, apathy occurs when the systems that generate and control voluntary actions are altered; 3. These systems are mostly represented by the different subregions embedded in the Prefrontal cortex (PFC) and in the basal ganglia regions that are closely connected with the PFC; 4. In consequence, clinically, apathy is a prefrontal syndrome either due to direct lesions of the PFC or to lesions of basal ganglia areas that are closely related to the PFC; 5. Apathy is not a single entity but rather heterogeneous. Several different mechanisms may lead to apathy; Because there are several anatomical-functional prefrontal-basal ganglia circuits, the underlying mechanisms responsible for apathy may differ according to which prefrontal-basal ganglia circuit is affected; 6. In this context, apathy is the macroscopic results of the disruption of one or several elementary steps necessary for goal-directed behavior that are subserved by different prefrontal-basal ganglia circuits; 7. Intense apathy is related to caudate nucleus and GPi, disrupting associative and limbic pathways from/to the PFC; 8. in progressive supranuclear palsy (PSP) and focal lesions (caudate nuclei, GPi), apathy may be due to a loss of PFC activation; 9. In Parkinson's disease (PD), apathy may be due to a loss of signal focalization; 10. More globally, we propose that apathy may be explained by the impact of lesions or dysfunctions of the BG, because these lesions or dysfunctions lead to a loss of amplification of the relevant signal and/or to a loss of temporal and spatial focalization, both of which result in a diminished extraction of the relevant signal within the frontal cortex, thereby inhibiting the capacity of the frontal cortex to select, initiate, maintain and shift programs of action.

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“…In the later stages of the disease, MSA patients also develop cortical metabolic reductions [20]. PSP patients have been found to have metabolic reductions in cortical regions, including the anterior cingulate gyrus and inferior frontal gyrus in addition to caudate nucleus and midbrain [21]. These findings suggest that profound uptake reductions in the frontal cortex, striatum, and midbrain may be relatively specific for the diagnosis of PSP.…”

Section: Vesicular Monoamine Transportermentioning

confidence: 99%

Neuroimaging of Parkinson’s disease and atypical parkinsonism

Zgaljardic

Feigin

2004

Curr Neurol Neurosci Rep

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The basal ganglia and its associated circuitry can be assessed with a variety of neuroimaging methods that can provide information regarding specific neurotransmitter systems, the functional activity of brain regions, and the structural integrity of these regions. In Parkinson's disease (PD) and related atypical parkinsonian syndromes (APS), these imaging methods may be useful for many reasons, including aiding in differential diagnosis and measuring the efficacy of new therapies. This paper reviews recent developments in the application of neuroimaging to the assessment of PD and related APS.

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Voxel-based comparison of regional cerebral glucose metabolism between PSP and corticobasal degeneration

Cited by 85 publications

References 16 publications

¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

Apathy and the basal ganglia

Neuroimaging of Parkinson’s disease and atypical parkinsonism

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Voxel-based comparison of regional cerebral glucose metabolism between PSP and corticobasal degeneration

Cited by 85 publications

References 16 publications

18F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

18F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

Apathy and the basal ganglia

Neuroimaging of Parkinson’s disease and atypical parkinsonism

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Product

Resources

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¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment