Decreased Basal Ganglia Volume in Cerebral Amyloid Angiopathy
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Background and Purpose Cerebral amyloid angiopathy (CAA) is a common pathology of the leptomeningeal and cortical small vessels associated with hemorrhagic and non-hemorrhagic brain injury. Given previous evidence for CAA-related loss of cortical thickness and white matter volume, we hypothesized that CAA might also cause tissue loss in the basal ganglia. Methods We compared basal ganglia volumes expressed as a percentage of total intracranial volume (pBGV) of non-demented patients with sporadic and hereditary CAA to age-matched healthy control (HC) and Alzheimer’s disease (AD) cohorts. Results Patients with sporadic CAA had lower pBGV (n=80, 1.16%±0.14%) compared to HC (n=80, 1.30%±0.13%, P<0.0001) and AD patients (n=80, 1.23%±0.11%, P=0.001). Similarly, patients with hereditary CAA demonstrated lower pBGV (n=25, 1.26%±0.17%) compared to their matched HC (n=25, 1.36%±0.15%, P=0.036). Using a measurement of normalized basal ganglia width developed for analysis of clinical-grade magnetic resonance images, we found smaller basal ganglia width in patients with CAA-related lobar intracerebral hemorrhage (ICH; n=93, 12.35±1.47) compared to age-matched patients with hypertension-related deep ICH (n=93, 13.46±1.51, P<0.0001) or HC (n=93, 15.45±1.22, P<0.0001). Within the sporadic CAA research cohort, decreased basal ganglia volume was independently correlated with greater cortical gray matter atrophy (r=0.45, P<0.0001), increased basal ganglia fractional anisotropy (r=–0.36, P=0.001), and worse performance on language processing (r=0.35, P=0.003), but not with cognitive tests of executive function or processing speed. Conclusions These findings suggest an independent effect of CAA on basal ganglia tissue loss, indicating a novel mechanism for CAA-related brain injury and neurologic dysfunction
Abstract
Background and Purpose Cerebral amyloid angiopathy (CAA) is a common pathology of the leptomeningeal and cortical small vessels associated with hemorrhagic and non-hemorrhagic brain injury. Given previous evidence for CAA-related loss of cortical thickness and white matter volume, we hypothesized that CAA might also cause tissue loss in the basal ganglia. Methods We compared basal ganglia volumes expressed as a percentage of total intracranial volume (pBGV) of non-demented patients with sporadic and hereditary CAA to age-matched healthy control (HC) and Alzheimer’s disease (AD) cohorts. Results Patients with sporadic CAA had lower pBGV (n=80, 1.16%±0.14%) compared to HC (n=80, 1.30%±0.13%, P<0.0001) and AD patients (n=80, 1.23%±0.11%, P=0.001). Similarly, patients with hereditary CAA demonstrated lower pBGV (n=25, 1.26%±0.17%) compared to their matched HC (n=25, 1.36%±0.15%, P=0.036). Using a measurement of normalized basal ganglia width developed for analysis of clinical-grade magnetic resonance images, we found smaller basal ganglia width in patients with CAA-related lobar intracerebral hemorrhage (ICH; n=93, 12.35±1.47) compared to age-matched patients with hypertension-related deep ICH (n=93, 13.46±1.51, P<0.0001) or HC (n=93, 15.45±1.22, P<0.0001). Within the sporadic CAA research cohort, decreased basal ganglia volume was independently correlated with greater cortical gray matter atrophy (r=0.45, P<0.0001), increased basal ganglia fractional anisotropy (r=–0.36, P=0.001), and worse performance on language processing (r=0.35, P=0.003), but not with cognitive tests of executive function or processing speed. Conclusions These findings suggest an independent effect of CAA on basal ganglia tissue loss, indicating a novel mechanism for CAA-related brain injury and neurologic dysfunction
참고문헌 (40)
- Wardlaw JM, "Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration", Lancet Neurol, 12, pp.822~838 (2013)
- Nitkunan A, "Brain atrophy and cerebral small vessel disease : a prospective follow-up study", Stroke, 42, pp.133~138 (2011)
- Ikram MK, "Retinal vascular calibers associate differentially with cerebral gray matter and white matter atrophy", Alzheimer Dis Assoc Disord, 27, pp.351~355 (2013)
- Brundel M, "Cerebral cortical thickness in patients with type 2 diabetes", J Neurol Sci, 299, pp.126~130 (2010)
- Fotiadis P, "Cortical atrophy in patients with cerebral amyloid angiopathy : a case-control study", Lancet Neurol, 15, pp.811~819 (2016)
- Gurol ME, "Cerebral amyloid angiopathy burden associated with leukoaraiosis : a positron emission tomography", magnetic resonance imaging study, 2013, pp.73, 529~536
- Fotiadis P, "White matter atrophy in cerebral amyloid angiopathy", Neurology, 95, pp.e554~ (2020)
- Salat DH, "White matter alterations in cerebral amyloid angiopathy measured by diffusion tensor imaging", Stroke, 37, pp.1759~1764 (2006)
- Reijmer YD, "Structural network alterations and neurological dysfunction in cerebral amyloid angiopathy", Brain (2015)
- Soontornniyomkij V, "Cerebral microinfarcts associated with severe cerebral beta-amyloid angiopathy", Brain Pathol, 20, pp.459~467 (2010)
- Auriel E, "Microinfarct disruption of white matter structure : a longitudinal diffusion tensor analysis", Neurology, 83, pp.182~188 (2014)
- Dumas A, "Functional magnetic resonance imaging detection of vascular reactivity in cerebral amyloid angiopathy", Ann Neurol, 72, pp.76~81 (2012)
- Peca S, "Neurovascular decoupling is associated with severity of cerebral amyloid angiopathy", Neurology, 81, pp.1659~1665 (2013)
- Mink JW, "The basal ganglia and involuntary movements : impaired inhibition of competing motor patterns", Arch Neurol, 60, pp.1365~1368 (2003)
- Foerde K, "The role of the basal ganglia in learning and memory : insight from Parkinson’s disease", Neurobiol Learn Mem, 96, pp.624~636 (2011)
- Booth JR, "The role of the basal ganglia and cerebellum in language processing", Brain Res, 1133, pp.136~144 (2007)
- Tanaka SC, "Prediction of immediate and future rewards differentially recruits cortico-basal ganglia loops", Nat Neurosci, 7, pp.887~893 (2004)
- Ashar YK, "Empathic care and distress : predictive brain markers and dissociable brain systems", Neuron, 94, pp.1263~1273 (2017)
- Tinaz S, "Focal cortical and subcortical atrophy in early Parkinson’s disease", Mov Disord, 26, pp.436~441 (2011)
- Cordato NJ, "Regional brain atrophy in progressive supranuclear palsy and Lewy body disease", Ann Neurol, 47, pp.718~728 (2000)
- Aylward EH, "Longitudinal change in basal ganglia volume in patients with Huntington’s disease", Neurology, 48, pp.394~399 (1997)
- Hanganu A, "Neuroimaging studies of striatum in cognition part II : Parkinson’s disease", Front Syst Neurosci, 9, pp.138~ (2015)
- Greenberg SM, "Diagnosis of cerebral amyloid angiopathy : evolution of the Boston criteria", Stroke, 49, pp.491~497 (2018)
- Jack CR Jr, "The Alzheimer’s Disease Neuroimaging Initiative(ADNI) : MRI methods", J Magn Reson Imaging, 27, pp.685~691 (2008)
- van Rooden S, "Descriptive analysis of the Boston criteria applied to a Dutch-type cerebral amyloid angiopathy population", Stroke, 40, pp.3022~3027 (2009)
- Pasi M, "Distribution of lacunes in cerebral amyloid angiopathy and hypertensive small vessel disease", Neurology, 88, pp.2162~2168 (2017)
- Fischl B, "Measuring the thickness of the human cerebral cortex from magnetic resonance images", Proc Natl Acad Sci U S A, 97, pp.11050~11055 (2000)
- Lee MJ, "Quantitative validation of a visual rating scale for defining high-iron putamen in patients with multiple system atrophy", Front Neurol, 10, pp.1014~ (2019)
- Case NF, "Cerebral amyloid angiopathy is associated with executive dysfunction and mild cognitive impairment", Stroke, 47, pp.2010~2016 (2016)
- Selden N, "Human striatum : the distribution of neurofibrillary tangles in Alzheimer’s disease", Brain Res, 648, pp.327~331 (1994)
- Gray F, "Leukoencephalopathy in diffuse hemorrhagic cerebral amyloid angiopathy", Ann Neurol, 18, pp.54~59 (1985)
- Smith EE, "MRI markers of small vessel disease in lobar and deep hemispheric intracerebral hemorrhage", Stroke, 41, pp.1933~1938 (2010)
- Fisher CM, "Pathological observations in hypertensive cerebral hemorrhage", J Neuropathol Exp Neurol, 30, pp.536~550 (1971)
- Werring DJ, "Diffusion tensor imaging of lesions and normal-appearing white matter in multiple sclerosis", Neurology, 52, pp.1626~1632 (1999)
- Douaud G, "In vivo evidence for the selective subcortical degeneration in Huntington’s disease", Neuroimage, 46, pp.958~966 (2009)
- Hasan KM, "Caudate nuclei volume, diffusion tensor metrics, and T(2) relaxation in healthy adults and relapsing-remitting multiple sclerosis patients: implications for understanding gray matter degeneration", J Magn Reson Imaging, 29, pp.70~77 (2009)
- Aylward EH, "Regional atrophy associated with cognitive and motor function in prodromal Huntington disease", J Huntingtons Dis, 2, pp.477~489 (2013)
- Gurol ME, "Plasma beta-amyloid and white matter lesions in AD, MCI, and cerebral amyloid angiopathy", Neurology, 66, pp.23~29 (2006)
- Maat-Schieman ML, "Hereditary cerebral hemorrhage with amyloidosis(Dutch) : a model for congophilic plaque formation without neurofibrillary pathology", Acta Neuropathol, 88, pp.371~378 (1994)
- Greenberg SM, "Outcome markers for clinical trials in cerebral amyloid angiopathy", Lancet Neurol, 13, pp.419~428 (2014)
