Please wait a minute...
Journal of Neurorestoratology  2019, Vol. 7 Issue (2): 63-69    doi: 10.26599/JNR.2019.9040007
Research Article     
Associated factors of early neurological deterioration in isolated acute lacunar infarction in basal ganglia
Honghao Man(✉), Yuhua Bi, Yongpeng Yu, Shengwu Wang, Zhenming Zhao, Xiaohong Qiao, Weiping Ju
Department of Neurology, Weihai Central Hospital Affiliated to Qingdao University, Weihai, Shandong 264400, China
Download: PDF (668 KB)      HTML
Export: BibTeX | EndNote (RIS)      

Abstract  Objective:

To investigate, in basal ganglia, the factors associated with early neurological deterioration (END) of isolated acute lacunar infarction.

Methods:

167 patients, in the retrospective group, with isolated acute lacunar infarction in basal ganglia, were defined by magnetic resonance imaging (MRI). The National Institutes of Health Stroke Scale (NIHSS) defined early neurological deterioration as increases of ≥ 2 within 72 hours following admission. Baseline variables predicting END were investigated with multivariate logistic regression analysis.

Results:

In the study, END occurred in 42 (25.15%) patients. Lesions located in posterior limb of internal capsule were independent risk factors for END (P < 0.01). Associated with END were the age of onset, history of cerebral infarction, history of diabetes, systolic blood pressure at admission and lesions of cerebral white matter. This presented significant differences (P < 0.05). With or without diabetes and different lesion location at varying layers and inter-layers, single-factor and multi-factor analysis revealed no effect on the association between positive ENT and age, history of stroke, white matter. Previous history of stroke, pathological changes of white matter, and age of onset, correlates with END which showed significant difference (P < 0.05).

Conclusions:

There is a close relationship between the lesion location and other related factors, such as lesions of cerebral white matter, history of cerebral infarction, history of diabetes and age, etc. and END in patients with isolated acute lacunar infarction in basal ganglia. Protective factors of END included age ≥ 65, high systolic pressure, stroke history, cerebral white matter lesions in our study.



Key wordsbrain ischemic tolerance      lacunar infarction      risk factor     
Received: 05 August 2018      Published: 22 July 2019
Corresponding Authors: Honghao Man   
Cite this article:

Honghao Man, Yuhua Bi, Yongpeng Yu, Shengwu Wang, Zhenming Zhao, Xiaohong Qiao, Weiping Ju. Associated factors of early neurological deterioration in isolated acute lacunar infarction in basal ganglia. Journal of Neurorestoratology, 2019, 7: 63-69.

URL:

http://jnr.tsinghuajournals.com/10.26599/JNR.2019.9040007     OR     http://jnr.tsinghuajournals.com/Y2019/V7/I2/63

Variable END negativeEND positivet/χ2 valueP value
Age< 6545 (66.18%)23 (33.82%)4.5840.032
≥ 6580 (80.81%)19 (19.19%)
GenderMale67 (72.83%)25 (27.17%)0.4460.504
Female58 (77.33%)17 (22.67%)
NIHSS score at admission1.96 ± 0.572.08 ± 0.451.2450.217
Site of infarctionVentral28 (82.35%)6 (17.65%)6.9690.031
Medial43 (83.31%)8 (15.69%)
Dorsal54 (65.85%)28 (34.15%)
Systolic blood pressure (mmHg)149.32 ± 15.41143.68 ± 14.89?2.0780.040
Diastolic blood pressure (mmHg)83.97 ± 11.1285.49 ± 9.970.7920.433
HypertensionNo34 (79.07%)9 (20.93%)0.5480.459
Yes91 (73.39%)33 (26.61%)
Diabetes mellitus (DM)No90 (73.77%)32 (26.23%)0.2800.596
Yes35 (77.78%)10 (22.22%)
Ever smokerNo77 (74.76%)26 (25.24%)0.3480.555
Yes38 (70.37%)16 (29.63%)
Alcohol drinkingNo54 (76.06%)17 (23.94%)0.0950.757
Yes71 (73.96%)25 (26.04%)
History of strokeNo76 (69.09%)34 (30.91%)5.6790.017
Yes49 (85.96%)8 (14.04%)
Homocysteine (μmol/L)9.12 ± 2.899.67 ± 2.561.0970.274
High density lipoprotein cholesterol (mmol/L)1.18 ± 0.201.22 ± 0.171.1720.246
Low-density lipoproteins (mmol/L)2.68 ± 0.742.57 ± 0.82?0.8150.419
Serum creatinine (mmol/L)72.69 ± 20.8673.83 ± 19.710.3180.757
Serum uric acid (mmol/L)319.15 ± 78.23311.70 ± 86.26?0.5270.604
C-reactive protein (mmol/L)0.98 ± 0.181.13 ± 0.214.482< 0.001
Admission blood glucose (mmol/L)6.35 ± 2.177.34 ± 2.262.5340.012
LeukoencephalopathyNo72 (67.92%)34 (32.08%)7.3940.007
Yes53 (86.89%)8 (13.11%)
Table 1General information of END positive and negative patients.
VariableβSEWaldP valueOR value95% CI
Agea?0.6720.2558.6370.0260.8310.422~0.950
Site of infarction9.0850.006
Medialb0.63340.4395.5320.1721.2240.834~1.926
Dorsalb2.5980.82612.0890.0014.6872.185~12.239
Systolic blood pressure–0.2860.0976.9030.0420.5690.334~0.8892
History of stroke–1.2350.3388.5310.0260.7970.598~0.964
C-reactive protein0.5820.1154.0640.2851.0030.851~1.461
Admission blood glucose0.3390.0828.0120.0241.5311.143~1.982
Leukoencephalopathyc–1.5390.67310.1370.0030.9630.885~0.997
Table 2Multivariate logistic regression analyses of significant risk factors for END.
VariableAgeStroke historyLeukoencephalopathy
≥65<65WithWithoutWithWithout
DMNOa0.892 (0.334~0.926)1.384 (1.029~2.671)0.764 (0.589~0.897)1.183 (1.002~1.639)0.808 (0.773~0.934)1.205 (1.137~1.689)
YESb0.711 (0.389~0.871)1.038 (1.071~2.394)0.708 (0.435~0.826)1.267 (1.317~1.925)0.724 (0.539~0.894)1.178 (1.089~2.006)
SIVentralc0.734 (0.689~1.832)1.591 (1.257~2.039)0.938 (0.572~0.985)1.083 (1.061~2.192)0.831 (0.702~0.929)1.282 (1.029~1.591)
Mediald0.972 (0.681~0.994)1.432 (1.115~2.447)0.793 (0.618~0.906)1.256 (1.097~2.058)0.794 (0.605~0.883)1.539 (1.373~1.992)
Dorsale0.989 (0.683~0.998)2.385 (1.639~4.159)0.893 (0.694~0.949)3.281 (1.773~5.201)0.835 (0.772~0.972)2.338 (1.524~4.384)
Table 3The correlation between END positive and age, stroke history or leukoencephalopathy.
[1]   Nakase T, Yamamoto Y, Takagi M, et al. The impact of diagnosing branch atheromatous disease for predicting prognosis. J Stroke Cerebrovasc Dis. 2015, 24(10): 2423-2428.
[2]   Steinke W, Ley SC. Lacunar stroke is the major cause of progressive motor deficits. Stroke. 2002, 33(6): 1510-1516.
[3]   Adams HP, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Stroke, 1993, 24(1): 35-41.
[4]   Jeong HG, Kim BJ, Yang MH, et al. Neuroimaging markers for early neurologic deterioration in single small subcortical infarction. Stroke. 2015, 46(3): 687-691.
[5]   Lee J, Albers GW, Marks MP, et al. Capsular warning syndrome caused by middle cerebral artery stenosis. J Neurol Sci. 2010, 296(1/2): 115-120.
[6]   Cohen JE, Rabinstein A, Gomori JM, et al. Capsular warning syndrome and crescendo lacunar strokes after atherosclerotic stenosis of the recurrent artery of Heubner. J Clin Neurosci. 2012, 19(12): 1730-1733.
[7]   Del Bene A, Palumbo V, Lamassa M, et al. Progressive lacunar stroke: Review of mechanisms, prognostic features, and putative treatments. Int J Stroke. 2012, 7(4): 321-329.
[8]   Yi XY, Wang C, Liu P, et al. Antiplatelet drug resistance is associated with early neurological deterioration in acute minor ischemic stroke in the Chinese population. J Neurol. 2016, 263(8): 1612-1619.
[9]   Chen ZL, Li W, Sun W, et al. Correlation study between small vessel disease and early neurological deterioration in patients with mild/moderate acute ischemic stroke. Int J Neurosci. 2017, 127(7): 579-585.
[10]   Zeynalov E, Doré S. Low doses of carbon monoxide protect against experimental focal brain ischemia. Neurotox Res. 2009, 15(2): 133-137.
[11]   Ziegler G, Freyer D, Harhausen D, et al. Blocking TLR2 in vivo protects against accumulation of inflammatory cells and neuronal injury in experimental stroke. J Cereb Blood Flow Metab. 2011, 31(2): 757-766.
[12]   Kitagawa K, Matsumoto M, Tagaya M, et al. ‘Ischemic tolerance’ phenomenon found in the brain. Brain Res. 1990, 528(1): 21-24.
[13]   Caplan LR. Do transient ischemic attacks have a neuroprotective effect? Neurology. 2000, 55(10): 1596.
[14]   Takuwa H, Masamoto K, Yamazaki K, et al. Long-term adaptation of cerebral hemodynamic response to somatosensory stimulation during chronic hypoxia in awake mice. J Cereb Blood Flow Metab. 2013, 33(5): 774-779.
[15]   Gao B, Zhang XY, Han R, et al. The endoplasmic reticulum stress inhibitor salubrinal inhibits the activation of autophagy and neuroprotection induced by brain ischemic preconditioning. Acta Pharmacol Sin. 2013, 34(5): 657-666.
[16]   Gamdzyk M, Ma?ek M, Bratek E, et al. Hyperbaric oxygen and hyperbaric air preconditioning induces ischemic tolerance to transient forebrain ischemia in the gerbil. Brain Res. 2016, 1648(Pt A): 257-265.
[17]   Wang HF, Xia HH, Qin JI, et al. The role of adenosine deaminase in the electroacupuncture preconditioning induced rapid tolerance to focal cerebral ischemia. Zhongguo Zhongxiyi Jiehe Zazhi. 2013, 33(2): 235-239.
[18]   Peng B, Guo QL, He ZJ, et al. Remote ischemic postconditioning protects the brain from global cerebral ischemia/ reperfusion injury by up-regulating endothelial nitric oxide synthase through the PI3K/Akt pathway. Brain Res. 2012, 1445: 92-102.
[19]   Brown IR. Heat shock proteins and protection of the nervous system. Ann N Y Acad Sci. 2007, 1113: 147-158.
[20]   Bigdeli MR, Khoshbaten A. In vivo preconditioning with normobaric hyperoxia induces ischemic tolerance partly by triggering tumor necrosis factor-alpha converting enzyme/ tumor necrosis factor-alpha/nuclear factor-kappaB. Neuroscience. 2008, 153(3): 671-678.
[21]   Noguchi CT, Asavaritikrai P, Teng RF, et al. Role of erythropoietin in the brain. Crit Rev Oncol Hematol. 2007, 64(2): 159-171.
[1] Xue Peng, Jianhua Zhao, Junli Liu, Shaomin Li. Advances in biomarkers of cerebral small vessel disease[J]. Journal of Neurorestoratology, 2019, 07(4): 171-183.