Frontal atrophy correlates with behavioural changes in progressive supranuclear palsy

Cordato, Nicholas J.; Pantelis, Christos; Halliday, Glenda M.; Velakoulis, Dennis; Wood, Stephen J.; Stuart, G. W.; Currie, Jay D.; Soo, Mark; Olivieri, Gloria; Broe, G. A.; Morris, John G.

doi:10.1093/brain/awf082

Cited by 110 publications

(54 citation statements)

References 47 publications

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“…Another small (n=6) MRI study found significant reductions in striatal volume in PSP patients (Schulz et al, 1999). Cordato et al (2002) identified 15% reduction in caudate volume (normalized for intracranial volume) in a PSP sample (n=21), but this was not significant once corrected for whole brain size. The Schulz et al (1999) study is therefore the only study to our knowledge that has successfully quantified previously pathologically observed striatal atrophy in PSP in vivo .…”

Section: Introductionmentioning

confidence: 90%

“…Macroscopic atrophy of the frontal cortex (Cordato et al, 2002) and subcortical structures (Schulz 1999; Schrag et al, 2000) distinguishes PSP from other parkinsonian syndromes on MRI. Subcortical atrophy in PSP affects the midbrain (particularly the ventral tegmentum), neostriatum, mamillary bodies and the superior cerebellar peduncle (Schrag et al, 2000), with the neostriatum and midbrain involved in frontostriatal circuits.…”

Section: Introductionmentioning

confidence: 99%

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Morphometric analysis of subcortical structures in progressive supranuclear palsy: In vivo evidence of neostriatal and mesencephalic atrophy

Looi

Macfarlane

Walterfang

et al. 2011

Psychiatry Research: Neuroimaging

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Progressive supranuclear palsy (PSP) is a neurodegenerative disease characterized by gait and postural disturbance, gaze palsy, apathy, decreased verbal fluency and dysexecutive symptoms, with some of these clinical features potentially having origins in degeneration of frontostriatal circuits and the mesencephalon. This hypothesis was investigated by manual segmentation of the caudate and putamen on MRI scans, using previously published protocols, in 15 subjects with PSP and 15 healthy age-matched controls. Midbrain atrophy was assessed by measurement of mid-sagittal area of the midbrain and pons. Shape analysis of the caudate and putamen was performed using spherical harmonics (SPHARM-PDM, University of North Carolina). The sagittal pons area/midbrain area ratio (P/M ratio) was significantly higher in the PSP group, consistent with previous findings. Significantly smaller striatal volumes were found in the PSP group – putamina were 10% smaller and caudate volumes were 17% smaller than in controls after controlling for age and intracranial volume. Shape analysis revealed significant shape deflation in PSP in the striatum, compared to controls; with regionally significant change relevant to frontostriatal and corticostriatal circuits in the caudate. Thus, in a clinically diagnosed and biomarker-confirmed cohort with early PSP, we demonstrate that neostriatal volume and shape are significantly reduced in vivo. The findings suggest a neostriatal and mesencephalic structural basis for the clinical features of PSP leading to frontostriatal and mesocortical-striatal circuit disruption.

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Section: Introductionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Morphometric analysis of subcortical structures in progressive supranuclear palsy: In vivo evidence of neostriatal and mesencephalic atrophy

Looi

Macfarlane

Walterfang

et al. 2011

Psychiatry Research: Neuroimaging

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“…This might suggest that either frontal lobe atrophy occurs early in the course of the disease as suggested in previous cross-sectional studies 14 or that the pattern of volume loss remains consistent into the latter stages of the disease. Serial imaging in the early stages may show accelerated rates of atrophy in areas specific to PSP and this technique may prove useful in differentiating PSP from other akinetic-rigid syndromes.…”

Section: Commentmentioning

confidence: 58%

Pathological substrate for regional distribution of increased atrophy rates in progressive supranuclear palsy

Paviour¹

2004

Journal of Neurology, Neurosurgery & Psychiatry

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Background: Most magnetic resonance imaging (MRI) studies of progressive supranuclear palsy (PSP) are crosssectional and lack post mortem confirmation of the diagnosis. MRI features described previously in PSP correspond to regions of pathological involvement demonstrated in separate studies, but serial MRI with pathological follow up has not been undertaken. Objective: To investigate whether regions of increased atrophy rates demonstrated in PSP during life using fluid registered serial MRI correspond with pathological findings in confirmed PSP. Methods: A 59 year old male presented with a six month history of balance problems and dysarthria. He had a symmetrical, levodopa unresponsive akinetic-rigid syndrome with a vertical supranuclear gaze palsy. A clinical diagnosis of probable PSP was made. His disease progressed relentlessly and he died five years after onset. Two serial MRI scans undertaken during life were reviewed and fluid (non-linear) registration of the images carried out. Post mortem histopathological analysis of the brain was undertaken to definitively confirm the diagnosis and compare regional pathology with the serial imaging. Results: Fluid registration demonstrated greatest rates of atrophy in the brainstem and frontal cortex, in keeping with the distribution of pathology seen at autopsy. Conclusion: Fluid registration of serial MRI allows the topography and rates of regional atrophy in PSP to be delineated in life. Atrophy patterns correlated well with regional pathological load. These observations suggest that serial MRI with registration may help differentiate PSP from clinically similar conditions and supports its use as a surrogate marker of disease progression.

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“…The inconsistency of conventional MRI modalities may be derived from the motion artifacts and image ghosting caused by the motor impairments and tremor associated with PD. Several studies found no difference in whole brain volumetric measurements in PD patients when compared to age matched healthy controls 174–176 . Two longitudinal studies, however, report an increased rate of annual brain volume loss and increased cerebral gray matter atrophy in PD patients 177,178 .…”

Section: Parkinson’s Diseasementioning

confidence: 99%

Examining the Relationship between Head Trauma and Neurodegenerative Disease: A Review of Epidemiology, Pathology and Neuroimaging Techniques

Sundman

Hall

Chen

2014

J Alzheimers Dis Parkinsonism

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Traumatic brain injuries (TBI) are induced by sudden acceleration-deceleration and/or rotational forces acting on the brain. Diffuse axonal injury (DAI) has been identified as one of the chief underlying causes of morbidity and mortality in head trauma incidents. DAIs refers to microscopic white matter (WM) injuries as a result of shearing forces that induce pathological and anatomical changes within the brain, which potentially contribute to significant impairments later in life. These microscopic injuries are often unidentifiable by the conventional computed tomography (CT) and magnetic resonance (MR) scans employed by emergency departments to initially assess head trauma patients and, as a result, TBIs are incredibly difficult to diagnose. The impairments associated with TBI may be caused by secondary mechanisms that are initiated at the moment of injury, but often have delayed clinical presentations that are difficult to assess due to the initial misdiagnosis. As a result, the true consequences of these head injuries may go unnoticed at the time of injury and for many years thereafter. The purpose of this review is to investigate these consequences of TBI and their potential link to neurodegenerative disease (ND). This review will summarize the current epidemiological findings, the pathological similarities, and new neuroimaging techniques that may help delineate the relationship between TBI and ND. Lastly, this review will discuss future directions and propose new methods to overcome the limitations that are currently impeding research progress. It is imperative that improved techniques are developed to adequately and retrospectively assess TBI history in patients that may have been previously undiagnosed in order to increase the validity and reliability across future epidemiological studies. The authors introduce a new surveillance tool ((Retrospective Screening of Traumatic Brain Injury Questionnaire, RESTBI) to address this concern.

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Frontal atrophy correlates with behavioural changes in progressive supranuclear palsy

Cited by 110 publications

References 47 publications

Morphometric analysis of subcortical structures in progressive supranuclear palsy: In vivo evidence of neostriatal and mesencephalic atrophy

Morphometric analysis of subcortical structures in progressive supranuclear palsy: In vivo evidence of neostriatal and mesencephalic atrophy

Pathological substrate for regional distribution of increased atrophy rates in progressive supranuclear palsy

Examining the Relationship between Head Trauma and Neurodegenerative Disease: A Review of Epidemiology, Pathology and Neuroimaging Techniques

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