Cerebral peduncle angle: Unreliable in differentiating progressive supranuclear palsy from other neurodegenerative diseases

Tipton, Philip W.; Konno, Tetsuo; Broderick, Daniel F.; Dickson, Dennis W.; Wszołek, Zbigniew K.

doi:10.1016/j.parkreldis.2016.08.009

Cited by 6 publications

(6 citation statements)

References 24 publications

(19 reference statements)

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“…130 In contrast, measurement of the cerebral peduncle angle (CPA) on axial view does not appear to be reliable in separating pathologically confirmed PSPS cases from CBD, MSA, and LBD. 131 Some skepticism remains regarding the utility of tau-PET in clinically diagnosed PSPS. Thus far, only a few small studies have been conducted, but it appears that 18 F-AV-1451 binding occurs primarily in subcortical structures, including the putamen, globus pallidus, subthalamic nucleus and dentate nucleus, as well as the midbrain, but not the neocortex or WM.…”

Section: Corticobasal Syndromementioning

confidence: 99%

Neuroimaging in Dementia

et al. 2017

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Although the diagnosis of dementia still is primarily based on clinical criteria, neuroimaging is playing an increasingly important role. This is in large part due to advances in techniques that can assist with discriminating between different syndromes. Magnetic resonance imaging remains at the core of differential diagnosis, with specific patterns of cortical and subcortical changes having diagnostic significance. Recent developments in molecular PET imaging techniques have opened the door for not only antemortem but early, even preclinical, diagnosis of underlying pathology. This is vital, as treatment trials are underway for pharmacological agents with specific molecular targets, and numerous failed trials suggest that earlier treatment is needed. This article provides an overview of classic neuroimaging findings as well as new and cutting-edge research techniques that assist with clinical diagnosis of a range of dementia syndromes, with an emphasis on studies using pathologically proven cases.

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Section: Corticobasal Syndromementioning

confidence: 99%

Neuroimaging in Dementia

et al. 2017

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“…The disease usually develops after the sixth decade of life, and the diagnosis is purely clinical. [ 70 ] The brainstem is one among the first regions affected in PSP and it is part of the sleep/circadian regulation network. [ 7 ] Symptoms of autonomic dysfunctions and GI dysfunction are common in patients with parkinsonian disorders such as PSP.…”

Section: Progressive Supranuclear Palsymentioning

confidence: 99%

Gastrointestinal dysfunction in idiopathic Parkinsonism: A narrative review

2016

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Currently, gastrointestinal (GI) dysfunctions in Parkinson's disease (PD) are well-recognized problems and are known to be the initial symptoms in the pathological process that eventually results in PD. Many types of PD-associated GI dysfunctions have been identified, including weight loss, nausea, hypersalivation, dysphagia, dyspepsia, abdominal pain, intestinal pseudo-obstruction, constipation, defecatory dysfunction, and small intestinal bacterial overgrowth. These symptoms can influence on other PD symptoms and are the second most significant predictor of the quality of life of these patients. Recognition of GI symptoms requires vigilance on the part of clinicians. Health-care providers should routinely ask direct questions about GI symptoms during office visits so that efforts can be directed at appropriate management of these distressing manifestations. Multiple system atrophy (MSA) and progressive supranuclear palsy are two forms of neurodegenerative Parkinsonism. Symptoms of autonomic dysfunctions such as GI dysfunction are common in patients with parkinsonian disorders. Despite recent progress in the recognition of GI dysfunctions, there are a few reviews on the management of GI dysfunction and GI symptoms in idiopathic Parkinsonism. In this review, the clinical presentation, pathophysiology, and treatment of each GI symptom in PD, MSA, and prostate-specific antigen will be discussed.

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“…Pathognomonic features alone are highly unreliable due to clinical heterogeneity between PD and APS phenotypes. 125 Parkinsonism can be divided into two types of neuropathologies: α-synucleinopathies (PD, MSA and DLB) and tauopathies (PSP and CBS). 126,127 α-synucleinopathies are characterised by αsynuclein in its stable unfolded oligomer state which is the main protein component of Lewy bodies and Lewy neurites and a significant hallmark of PD.…”

Section: Potential Therapeutic Biomarkers For Progressive Supranuclear Palsymentioning

confidence: 99%

“…133 However, Tipton et al could not form a conclusive distinction between PSP and other neurodegenerative diseases using measurements of the cerebellar peduncle angle (CPA). 125 MRPI is recommended for clinical use and has proven to perform better than P/M ratio to distinguish between PSP and PD patients. 161 MRI shows midbrain and superior cerebellar peduncles (SCPs) atrophy for PSP patients and pontine atrophy in MSA patients.…”

Section: Quattrone Et Al Introduces the Magnetic Resonance Parkinsonism Index (Mrpi) Formentioning

confidence: 99%

Novel Therapeutic Targets and Biomarkers for the Treatment of Progressive Supranuclear Palsy

Tyer¹,

Hill²

2020

Preprint

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Progressive supranuclear palsy (PSP) is a sporadic parkinsonism tauopathy characterised by the deposition of aggregations of abnormal, hyperphosphorylated four-repeat tau (4R-tau). A revised clinical diagnostic criterion for PSP allows early presentations for the full spectrum of clinical phenotypes to be recognised enabling doctors to make a more accurate diagnosis. The major genetic risk factor for sporadic PSP is a common variant in the gene encoding microtubule-associated protein tau (MAPT). Research into the biochemical and pathological pathways of tau is vital to improve the chances of developing an effective diagnostic biomarker to monitor tau pathogenesis. Neuroimaging biomarkers, such as tau PET ligands, are proving the most successful tool in providing a differential diagnosis between neurodegenerative disorders. There are currently no effective treatments for PSP, however tau-directed therapies in the last five years have rapidly advanced. Latest tau therapies are proposed to have disease-modifying effects by reducing toxic aggregations of tau through manipulating tau gene expression. After encouraging results from long awaited trials, additional funding is being injected into this field and with new results expected, this proves an exciting area for scientific discovery. This paper reviews advances in pathophysiology, diagnosis, biomarkers and disease-modifying therapeutic treatments for PSP.

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Cerebral peduncle angle: Unreliable in differentiating progressive supranuclear palsy from other neurodegenerative diseases

Cited by 6 publications

References 24 publications

Neuroimaging in Dementia

Neuroimaging in Dementia

Gastrointestinal dysfunction in idiopathic Parkinsonism: A narrative review

Novel Therapeutic Targets and Biomarkers for the Treatment of Progressive Supranuclear Palsy

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