Risk Factors for Aphasia in Cerebral Small Vessel Diseases

Author(s): Jiawei Xin, Xuanyu Huang*, Xiaodong Pan, Lin Lin, Mingyao Sun, Chen Liu, Qinyong Ye*.

Journal Name: Current Neurovascular Research

Volume 16 , Issue 2 , 2019

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Abstract:

Background: Lacunes and white matter hyperintensities (WMH) are two common findings seen on neuroimaging in patients with cerebral small vessel disease (cSVD). Clinically we observed that some patients with cSVD have aphasia through the language assessment scale. Our study aimed to explore the underlying risk factors for aphasia in cSVD patients.

Methods: This study retrospectively analyzed 38 patients, with and without aphasia, aged 50 or over, Chinese Han population, diagnosed as cSVD with lacunes and/or WMH. We collected demographic characteristics and vascular risk factors. The severity of WMH was assessed by the age related white matter changes (ARWMC) rating scale.

Results: Risk factors associated with aphasia were: lower education (p = 0.029), higher total cholesterol (TC) levels (p = 0.023), and higher low-density lipoprotein cholesterol (LDL-C) levels (p = 0.027). After controlling for age and sex, levels of TC (odds ratios, 1.96; 95% confidence interval, 1.06-3.62; p = 0.032) remained associated with aphasia independently.

Conclusion: High level of TC was significantly associated with a higher risk of aphasia in clinically silent cSVD patients. Early interventions including lipid-lowering treatment, cranial magnetic resonance imaging (MRI) and ARWMC rating scale should be performed. Further studies are needed to explore proper methods of prevention and treatment for aphasia in clinically silent cSVD patients, in addition to understanding the pathophysiological mechanism.

Keywords: Aphasia, cerebral Small Vessel Disease (cSVD), lacune, risk factors, White Matter Hyperintensities (WMH), neuroimaging.

[1]
Shi Y, Wardlaw JM. Update on cerebral small vessel disease: A dynamic whole-brain disease. Stroke Vasc Neurol 2016; 1(3): 83-92.
[2]
Wardlaw JM, Smith EE, Biessels GJ, et al. Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration. Lancet Neurol 2013; 12(8): 822-38.
[3]
Pantoni L. Cerebral small vessel disease: From pathogenesis and clinical characteristics to therapeutic challenges. Lancet Neurol 2010; 9(7): 689-701.
[4]
Vermeer SE, Longstreth WT, Koudstaal PJ. Silent brain infarcts: A systematic review. Lancet Neurol 2007; 6(7): 611-9.
[5]
Snowdon DA, Greiner LH, Mortimer JA, Riley KP, Greiner PA, Markesbery WR. Brain infarction and the clinical expression of Alzheimer disease: The Nun Study. JAMA 1997; 277(10): 813-7.
[6]
Vermeer SE, Prins ND, den Heijer T, Hofman A, Koudstaal PJ, Breteler MM. Silent brain infarcts and the risk of dementia and cognitive decline. N Engl J Med 2003; 348(13): 1215-22.
[7]
Fanning JP, Wong AA, Fraser JF. The epidemiology of silent brain infarction: A systematic review of population-based cohorts. BMC Med 2014; 12(1): 119.
[8]
Xiong YY, Mok V. Age-related white matter changes. J Aging Res 2011; 2011: 1-13.
[9]
Debette S, Markus H. The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: Systematic review and meta-analysis. BMJ 2010; 341: c3666.
[10]
Mok V, Srikanth V, Xiong Y, et al. Race-ethnicity and cerebral small vessel disease-comparison between Chinese and White populations Int J Stroke 2014; 9(Suppl A100): 36-42.
[11]
van Straaten EC, Scheltens P, Knol DL, et al. Operational definitions for the NINDS-AIREN criteria for vascular dementia. An interobserver study. Stroke 2003; 34(8): 1907-12.
[12]
Staekenborg SS, Van der Flier WM, Van Straaten EC, Lane R, Barkhof F, Scheltens P. Neurological signs in relation to type of cerebrovascular disease in vascular dementia. Stroke 2008; 39(2): 317-22.
[13]
Geschwind N. Disconnexion syndromes in animals and man: Part I. Neuropsychol Rev 2010; 20(2): 128-57.
[14]
den Ouden DB, Malyutina S, Basilakos A, et al. Cortical and structural-connectivity damage correlated with impaired syntactic processing in aphasia. Hum Brain Mapp 2019; 40(7): 2153-73.
[15]
Dickey L, Kagan A, Lindsay MP, Fang J, Rowland A, Black S. Incidence and profile of inpatient stroke-induced aphasia in Ontario, Canada. Arch Phys Med Rehabil 2010; 91(2): 196-202.
[16]
Berthier ML. Poststroke aphasia. Drugs Aging 2005; 22(2): 163-82.
[17]
Qihao G, Zhen H. Neuropsychological Assessment. Shanghai Scientific & Technical Publishers Shanghai 2013.
[18]
Mingyao S. Research on the standardization of Language Screening Test (LAST) in patients with stroke. J Neurol 2017; 264(2): 211-20.
[19]
Wolf PA, D’agostino RB, Belanger AJ, Kannel WB. Probability of stroke: A risk profile from the Framingham Study. Stroke 1991; 22(3): 312-8.
[20]
Flamand-Roze C, Falissard B, Roze E, et al. Validation of a new language screening tool for patients with acute stroke: The Language Screening Test (LAST). Stroke 2011; 42(5): 1224-9.
[21]
Vermeer SE, den Heijer T, Koudstaal PJ, Oudkerk M, Hofman A, Breteler MM. Incidence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study. Stroke 2003; 34(2): 392-6.
[22]
Longstreth W, Bernick C, Manolio TA, Bryan N, Jungreis CA, Price TR. Lacunar infarcts defined by magnetic resonance imaging of 3660 elderly people: The cardiovascular health study. Arch Neurol 1998; 55(9): 1217-25.
[23]
Geller J, Thye M, Mirman DJN. Estimating effects of graded white matter damage and binary tract disconnection on post-stroke language impairment. Neuroimage 2019; 189: 248-57.
[24]
Fazekas F, Kleinert R, Offenbacher H, et al. Pathologic correlates of incidental MRI white matter signal hyperintensities. Neurology 1993; 43(9): 1683.
[25]
Wahlund L-O, Barkhof F, Fazekas F, et al. A new rating scale for age-related white matter changes applicable to MRI and CT. Stroke 2001; 32(6): 1318-22.
[26]
Mahmood SS, Levy D, Vasan RS, Wang TJ. The Framingham heart study and the epidemiology of cardiovascular disease: A historical perspective. Lancet 2014; 383(9921): 999-1008.
[27]
Houston DK, Ding J, Lee JS, et al. Dietary fat and cholesterol and risk of cardiovascular disease in older adults: The health ABC study. Nutr Metab Cardiovasc Dis 2011; 21(6): 430-7.
[28]
Tippett DC, Hillis AE. Where are aphasia theory and management “headed”? F1000 Res 2017; 6: F1000.
[29]
Engelter ST, Gostynski M, Papa S, et al. Epidemiology of aphasia attributable to first ischemic stroke: Incidence, severity, fluency, etiology, and thrombolysis. Stroke 2006; 37(6): 1379-84.
[30]
Pedersen PM, Vinter K, Olsen TS. Aphasia after stroke: Type, severity and prognosis. The Copenhagen aphasia study. Cerebrovasc Dis 2004; 17(1): 35-43.
[31]
Laska A, Hellblom A, Murray V, Kahan T, Von Arbin M. Aphasia in acute stroke and relation to outcome. J Iinternal Med 2001; 249(5): 413-22.
[32]
Khan U, Porteous L, Hassan A, Markus HS. Risk factor profile of cerebral small vessel disease and its subtypes. J Neurol Neurosurg Psychiatry 2007; 78(7): 702-6.
[33]
Hassan A. Markers of endothelial dysfunction in lacunar infarction and ischaemic leukoaraiosis. Brain 2003; 126(2): 424-32.
[34]
Hassan A, Hunt BJ, O’sullivan M, et al. Homocysteine is a risk factor for cerebral small vessel disease, acting via endothelial dysfunction. Brain 2004; 127(1): 212-9.
[35]
Wardlaw JM, Allerhand M, Doubal FN, et al. Vascular risk factors, large-artery atheroma, and brain white matter hyperintensities. Neurology 2014; 82(15): 1331-8.
[36]
Dufouil C, de Kersaint–Gilly A, Besancon V, et al. Longitudinal study of blood pressure and white matter hyperintensities the EVA MRI cohort. Neurology 2001; 56(7): 921-6.
[37]
Dufouil C, Chalmers J, Coskun O, et al. Effects of blood pressure lowering on cerebral white matter hyperintensities in patients with stroke: the PROGRESS (Perindopril Protection Against Recurrent Stroke Study) Magnetic Resonance Imaging Substudy. Circulation 2005; 112(11): 1644-50.
[38]
Weber R, Weimar C, Blatchford J, et al. Telmisartan on top of antihypertensive treatment does not prevent progression of cerebral white matter lesions in the prevention regimen for effectively avoiding second strokes (PRoFESS) MRI substudy. Stroke 2012; 43(9): 2336-42.
[39]
Mok VC, Lam WW, Fan YH, et al. Effects of statins on the progression of cerebral white matter lesion: Post hoc analysis of the ROCAS (Regression of Cerebral Artery Stenosis) study. J Neurol 2009; 256(5): 750-7.
[40]
Bath PM, Wardlaw JM. Pharmacological treatment and prevention of cerebral small vessel disease: A review of potential interventions. Int J Stroke 2015; 10(4): 469-78.
[41]
Gerstenecker A, Lazar RM. Language recovery following stroke. Clin Neuropsychol 2019; 33(5): 928-47.
[42]
Hilari K, Behn N, Marshall J, et al. Adjustment with aphasia after stroke: Study protocol for a pilot feasibility randomised controlled trial for Supporting wellbeing through PEeR Befriending (SUPERB). Pilot Feasibility Stud 2019; 22; 5: 14.


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Article Details

VOLUME: 16
ISSUE: 2
Year: 2019
Page: [107 - 114]
Pages: 8
DOI: 10.2174/1567202616666190227202638
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