Abstract
Background: Stroke has always been considered as an urgent medical problem in every country in the world. Symptoms of stroke are varied, causing many disorders in movement, cognitive perception and social psychology. In which, language disorder is a common symptom and often leaves sequelae for patients. Cerebral infarction is a common type of stroke that causes language disorders.
Objectives: 1. To survey the types of language disorders in patients with cerebral infarction at the University of Medicine and Pharmacy Hospital; 2. To identify relevant factors between clinical, location, and size of lesions with types of language disorders.
Subjects and methods: Cross-sectional descriptive study on 30 patients with cerebral infarction who suffer from language disorders at The Stroke Center, Hue University of Medicine and Pharmacy Hospital from March 2024 to December 2024, assessment of language disorders using The Aphasia Rapid Test (ART).
Results: Patients ≥ 70 years old (70.0%). Male patients (70.0%), female patients (30.0%). Subacute cerebral infarction duration (43.3%). Hemispheric lesions were mainly left (70.0%), subcortical (53.3%). Middle cerebral artery lesions accounted for a high proportion (36.7%). Lesion size 0.5 - 15 mm (63.3%). The location of the lesions is divided by area/lobe with the highest rate of coronal radiata, followed by the temporal lobe, occipital lobe, interlobe and the lowest rate of lesions in the insula, caudate nucleus, cerebellum, brain stem, corpus callosum. The rate of aphasia types in patients with cerebral infarction is Trans-motor cortex (30.0%), Broca (23.2%), Conduction (16.7%), Wernicke (10.0%), Total/Trans-sensory cortex/Mixed Trans-cortex (6.7%), no Anomic aphasia. There is a relationship between the location of cortical/subcortical lesions and the type of aphasia p = 0.047 (< 0.05). The relationship between temporal lobe lesions and Wernicke aphasia (p = 0.014), the relationship between coronal ramus lesions and Conduction aphasia (p = 0.003), the relationship between frontal lobe lesions and Total aphasia (p = 0.034), the relationship between centrum semiovale lesions and Transmotor aphasia were statistically significant with p = 0.049.
Conclusion: Aphasia is a common complication of ischemic stroke, with transcortical motor aphasia accounting for the highest percentage at 30.0%, followed by Broca's aphasia at 23.2%. There is a correlation between the location of cortical/subcortical lesions and the type of aphasia.
| Published | 2025-12-25 | |
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| Issue | Vol. 15 No. 7 (2025) | |
| Section | Original Articles | |
| DOI | 10.34071/jmp.2025.7.32 | |
| Keywords | thất ngôn, nhồi máu não, vị trí tổn thương aphasia, stroke, location of lesions |

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Copyright (c) 2025 Hue Journal of Medicine and Pharmacy
Berge KE, Tian H, Graf GA, Yu L, Grishin NV, Li J, et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters. Science. 2000;290(5497):1771-5.
National Center for Biotechnology Information. ClinVar [Internet]. Bethesda (MD): National Library of Medicine (US); [cited 2025]. Sitosterolemia, ABCG5. Available from: https://www.ncbi.nlm.nih.gov/ clinvar/?term=Sitosterolemia%2C+ABCG5
National Center for Biotechnology Information. ClinVar [Internet]. Bethesda (MD): National Library of Medicine (US); [cited 2025]. Sitosterolemia, ABCG8. Available from: https://www.ncbi.nlm.nih.gov/ clinvar/?term=Sitosterolemia%2C+ABCG8
Genome Aggregation Database (gnomAD) [Internet]. Cambridge (MA): Broad Institute; [cited 2025]. ATP binding cassette subfamily G member 5 (ABCG5). Available from: https://gnomad.broadinstitute.org/gene/ ENSG00000138075?dataset=gnomad_r4
Lek M, Karczewski KJ, Minikel EV, Samocha KE, Banks E, Fennell T, et al. Analysis of protein-coding genetic variation in 60,706 humans. Nature. 2016;536(7616):285- 91.
Sakuma N, Tada H, Mabuchi H, Kawashiri MA, Takata M, Nohara A, et al. Lipoprotein Apheresis for Sitosterolemia. Ann Intern Med. 2017;167(12):896-9.
Kawamura R, Saiki H, Tada H, Takata M, Kawashiri MA, Nohara A, et al. Acute myocardial infarction in a 25-year-old woman with sitosterolemia. J Clin Lipidol. 2018;12(1):246-9.
Yamada Y, Sugi K, Gatate Y, Nakachi T. Premature Acute Myocardial Infarction in a Young Patient With Sitosterolemia. CJC Open. 2021;3(8):1085-8.
Genome Aggregation Database (gnomAD) [Internet]. Cambridge (MA): Broad Institute; [cited 2025]. ABCG5 ATP binding cassette subfamily G member 5 (v2.1). Available from: https://gnomad.broadinstitute.org/gene/ ENSG00000138075?dataset=gnomad_r2_1
National Center for Biotechnology Information. ClinVar [Internet]. Bethesda (MD): National Library of Medicine (US); [cited 2025]. VCV000005187.14 (p.His510Asn). Available from: https://www.ncbi.nlm.nih. gov/clinvar/?term=p.His510Asn
Do TT, Vu CD. Kiểu gen và kiểu hình của tăng Cholesterol máu tiên phát ở trẻ em. Tạp Chí Nghiên cứu Y học. 2021;138:37-41.
Lamiquiz-Moneo I, Baila-Rueda L, Bea AM, Jarauta E, Tejedor MT, Mateo-Gallego R, et al. ABCG5/G8 gene is associated with hypercholesterolemias without mutation in candidate genes and noncholesterol sterols. J Clin Lipidol. 2017;11(6):1432-40.
Park JH, Chung IH, Kim DH, Choi MH, Garg A. Sitosterolemia presenting with severe hypercholesterolemia and intertriginous xanthomas in a breastfed infant: case report and brief review. J Clin Endocrinol Metab. 2014;99(5):1512-8.
Tada H, Nohara A, Inazu A, Sakuma N, Mabuchi H, Kawashiri MA. Sitosterolemia, Hypercholesterolemia, and Coronary Artery Disease. J Atheroscler Thromb. 2018;25(9):783-9.





