A Case of Pathologically Confirmed Corticobasal Degeneration Initially Presenting as Progressive Supranuclear Palsy Syndrome

Chung, Eun Joo; Cho, Hwa Jin; Jang, Wooyoung; Hur, Dae Young; Kim, Yeong Seok; Lee, Kyung-Hwa; Kim, Sang Jin

doi:10.3346/jkms.2022.37.e183

Cited by 4 publications

(3 citation statements)

References 11 publications

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“…Other common pathologies include frontotemporal degeneration, Lewy body disease (LBD), Pick disease, and motor neuron disease. Of these neurodegenerative disorders that can be clinically diagnosed with CBS, PSP and CBD (particularly the PSP-like type) can exhibit significant pathological findings in the midbrain 17,18,24 . Although the number of subjects was small, we calculated the MUR values in patients clinically diagnosed with frontotemporal degeneration (n = 6) and LBD (n = 3) and found that the MUR values in the FTLT and LBD groups were roughly equivalent to those in the HC and AD groups (Supplement S1, http://links.lww.com/CNM/A428).…”

Section: Discussionmentioning

confidence: 99%

Detailed Assessment of 18F-THK5351 Distribution Pattern in the Midbrain: Comparison With Progressive Supranuclear Palsy and Corticobasal Syndrome

Ishibashi,

Kurihara,

Ihara

et al. 2023

Clin Nucl Med

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Background 18F-THK5351 PET is used to image ongoing astrogliosis by estimating monoamine oxidase B levels. 18F-THK5351 preferentially accumulates around the substantia nigra (SN) and periaqueductal gray (PG) in the midbrain under healthy conditions and exhibits a “trimodal pattern.” In progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS), the midbrain 18F-THK5351 uptake can be increased by astrogliosis, collapsing the “trimodal pattern.” We aimed to elucidate cases in which the “trimodal pattern” collapses in PSP and CBS. Patients and Methods Participants in the PSP (n = 11), CBS (n = 17), Alzheimer disease (n = 11), and healthy control (n = 8) groups underwent 18F-THK5351 PET. Volumes of interest (VOIs) were placed on the SN, PG, and their midpoints. The midbrain uptake ratio (MUR) was calculated to assess the trimodal pattern as follows: MUR = (VOI value on the midpoint)/(VOI value on the SN and PG). Approximately, the trimodal pattern can be identified at MUR <1 but not at MUR >1. Results Compared with the healthy control group, MUR significantly increased in the PSP (P < 0.01) and CBS (P < 0.01) groups, but was unchanged in the Alzheimer disease group (P = 0.10). In the PSP group, all patients, including 2 with mild symptoms and a short disease duration, showed MUR >1. In the CBS group, MUR varied widely. Conclusions In PSP, the trimodal pattern can collapse even in the early phase when symptoms are mild. In CBS, the trimodal pattern may or may not collapse depending on the underlying pathology.

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Section: Discussionmentioning

confidence: 99%

Detailed Assessment of 18F-THK5351 Distribution Pattern in the Midbrain: Comparison With Progressive Supranuclear Palsy and Corticobasal Syndrome

Ishibashi,

Kurihara,

Ihara

et al. 2023

Clin Nucl Med

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“…24 The patients with higher MUR values in the CBS group were expected to be attributed to PSP or CBD (particularly the PSP-like type) pathology. 29,33,35 Therefore, MUR is a helpful index for considering the underlying pathology in parkinsonian syndromes and is useful as an adjunct for the diagnosis of PSP.…”

Section: Corticobasal Syndromementioning

confidence: 99%

“…This is because CBS is a heterogeneous disorder consisting of various underlying pathologies, such as CBD, PSP, AD, FTLD‐TDP, and Lewy body disease 24 . The patients with higher MUR values in the CBS group were expected to be attributed to PSP or CBD (particularly the PSP‐like type) pathology 29,33,35 . Therefore, MUR is a helpful index for considering the underlying pathology in parkinsonian syndromes and is useful as an adjunct for the diagnosis of PSP.…”

Section: Neurodegenerative Disordersmentioning

confidence: 99%

Clinical application of MAO‐B PET using ¹⁸F‐THK5351 in neurological disorders

Ishibashi

2023

Geriatrics Gerontology Int

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Monoamine oxidase B (MAO‐B) is an enzyme localized to the outer mitochondrial membrane and highly concentrated in astrocytes. Temporal changes in regional MAO‐B levels can be used as an index of astrocytic proliferation, known as activated astrocytes or astrogliosis. MAO‐B is a marker to evaluate the degree of astrogliosis. Therefore, MAO‐B positron emission tomography (PET) is a powerful imaging technique for visualizing and quantifying ongoing astrogliosis through the estimate of regional MAO‐B levels. Each neurodegenerative disorder generally has a characteristic distribution pattern of astrogliosis secondary to neuronal loss and pathological protein aggregation. Therefore, by imaging astrogliosis, MAO‐B PET can be used as a neurodegeneration marker for identifying degenerative lesions. Any inflammation in the brain usually accompanies astrogliosis starting from an acute phase to a chronic phase. Therefore, by imaging astrogliosis, MAO‐B PET can be used as a neuroinflammation marker for identifying inflammatory lesions. MAO‐B levels are high in gliomas originating from astrocytes but low in lymphoid tumors. Therefore, MAO‐B PET can be used as a brain tumor marker for identifying astrocytic gliomas by imaging MAO‐B levels and distinguishing between astrocytic and lymphoid tumors. This review summarizes the clinical application of MAO‐B PET using 18F‐THK5351 as markers for neurodegeneration, neuroinflammation, and brain tumors in neurological disorders. Because we assume that MAO‐B PET is clinically applied to an individual patient, we focus on visual inspection of MAO‐B images at the individual patient level. Geriatr Gerontol Int 2023; ••: ••–••.

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Asymmetry in Atypical Parkinsonian Syndromes—A Review

Chunowski,

Madetko-Alster,

Alster

2024

JCM

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Background/Objectives: Atypical parkinsonian syndromes (APSs) are a group of neurodegenerative disorders that differ from idiopathic Parkinson’s disease (IPD) in their clinical presentation, underlying pathology, and response to treatment. APSs include conditions such as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), and dementia with Lewy bodies (DLB). These disorders are characterized by a combination of parkinsonian features and additional symptoms, such as autonomic dysfunction, supranuclear gaze palsy, and asymmetric motor symptoms. Many hypotheses attempt to explain the causes of neurodegeneration in APSs, including interactions between environmental toxins, tau or α-synuclein pathology, oxidative stress, microglial activation, and vascular factors. While extensive research has been conducted on APSs, there is a limited understanding of the symmetry in these diseases, particularly in MSA. Neuroimaging studies have revealed metabolic, structural, and functional abnormalities that contribute to the asymmetry in APSs. The asymmetry in CBS is possibly caused by a variable reduction in striatal D2 receptor binding, as demonstrated in single-photon emission computed tomography (SPECT) examinations, which may explain the disease’s asymmetric manifestation and poor response to dopaminergic therapy. In PSP, clinical dysfunction correlates with white matter tract degeneration in the superior cerebellar peduncles and corpus callosum. MSA often involves atrophy in the pons, putamen, and cerebellum, with clinical symmetry potentially depending on the symmetry of the atrophy. The aim of this review is to present the study findings on potential symmetry as a tool for determining potential neuropsychological disturbances and properly diagnosing APSs to lessen the misdiagnosis rate. Methods: A comprehensive review of the academic literature was conducted using the medical literature available in PubMed. Appropriate studies were evaluated and examined based on patient characteristics and clinical and imaging examination outcomes in the context of potential asymmetry. Results: Among over 1000 patients whose data were collected, PSP-RS was symmetrical in approximately 84% ± 3% of cases, with S-CBD showing similar results. PSP-P was symmetrical in about 53–55% of cases, while PSP-CBS was symmetrical in fewer than half of the cases. MSA-C was symmetrical in around 40% of cases. It appears that MSA-P exhibits symmetry in about 15–35% of cases. CBS, according to the criteria, is a disease with an asymmetrical clinical presentation in 90–99% of cases. Similar results were obtained via imaging methods, but transcranial sonography produced different results. Conclusions: Determining neurodegeneration symmetry may help identify functional deficits and improve diagnostic accuracy. Patients with significant asymmetry in neurodegeneration may exhibit different neuropsychological symptoms based on their individual brain lateralization, impacting their cognitive functioning and quality of life.

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A Case of Pathologically Confirmed Corticobasal Degeneration Initially Presenting as Progressive Supranuclear Palsy Syndrome

Cited by 4 publications

References 11 publications

Detailed Assessment of 18F-THK5351 Distribution Pattern in the Midbrain: Comparison With Progressive Supranuclear Palsy and Corticobasal Syndrome

Detailed Assessment of 18F-THK5351 Distribution Pattern in the Midbrain: Comparison With Progressive Supranuclear Palsy and Corticobasal Syndrome

Clinical application of MAO‐B PET using ¹⁸F‐THK5351 in neurological disorders

Asymmetry in Atypical Parkinsonian Syndromes—A Review

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A Case of Pathologically Confirmed Corticobasal Degeneration Initially Presenting as Progressive Supranuclear Palsy Syndrome

Cited by 4 publications

References 11 publications

Detailed Assessment of 18F-THK5351 Distribution Pattern in the Midbrain: Comparison With Progressive Supranuclear Palsy and Corticobasal Syndrome

Detailed Assessment of 18F-THK5351 Distribution Pattern in the Midbrain: Comparison With Progressive Supranuclear Palsy and Corticobasal Syndrome

Clinical application of MAO‐B PET using 18F‐THK5351 in neurological disorders

Asymmetry in Atypical Parkinsonian Syndromes—A Review

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Clinical application of MAO‐B PET using ¹⁸F‐THK5351 in neurological disorders