背景:中风通常会损害基底神经节,导致非典型和短暂的失语症,提示卒中后基底节失语(PSBGA)可能与不同的解剖结构损伤和功能重塑康复机制有关。基底神经节含有致密的白质束(WMTs)。因此,功能束的损伤可能是PSBGA发展的基本解剖学结构基础。
方法:我们首先使用Western失语症电池和神经心理学测试电池分析了28例患者和15例健康对照(HCs)中PSBGA的临床特征。此外,我们使用弥散磁共振成像扫描的差异纤维束造影研究了急性期的白质损伤.最后,我们在相关纤维束成像中使用多元回归模型来分析各种语言功能与WMT的定量各向异性(QA)之间的关系。
结果:与HC相比,PSBGA患者流畅性得分较低,理解(听觉单词识别和顺序命令),命名(对象命名和单词流畅性),阅读理解句子,迷你精神状态检查,和蒙特利尔认知评估,在卒中发病后7天内,汉密尔顿焦虑量表-17和汉密尔顿抑郁量表-17得分增加(P<0.05)。差异纤维束造影显示PSBGA患者的纤维受损,包括在call体的身体纤维中,左扣带束,左顶叶倾斜束,双侧上纵束II,双侧丘脑辐射束,左穹窿,胼胝体绒毡层,和镊子专业,与HC相比(FDR<0.02)。相关纤维束造影强调,更好的理解力与左额枕骨下束(IFOF)的较高QA相关,小调call体镊子,和左极限囊(FDR<0.0083)。命名与左IFOF的QA呈正相关,小镊子,左弓形束,和钩束囊(UF)(FDR<0.0083)。命名的单词流畅性也与镊子未成年人的QA呈正相关,左IFOF,和丘脑辐射束(FDR<0.0083)。此外,阅读与钳子未成年人的QA呈正相关,左IFOF,和UF(FDR<0.0083)。
结论:PSBGA的主要特征是命名的单词流畅性和保留的重复能力显着受损,以及情绪和认知功能障碍。边缘通路受损,位于左半球背侧的束,和左侧基底神经节通路参与PSBGA的发病机制。连接分析的结果进一步完善了与语言功能相关的高阶神经网络的当前功能定位模型。
BACKGROUND: Stroke often damages the basal ganglia, leading to atypical and transient aphasia, indicating that post-stroke basal ganglia aphasia (PSBGA) may be related to different anatomical structural damage and functional remodeling rehabilitation mechanisms. The basal ganglia contain dense white matter tracts (WMTs). Hence, damage to the functional tract may be an essential anatomical structural basis for the development of PSBGA.
METHODS: We first analyzed the clinical characteristics of PSBGA in 28 patients and 15 healthy controls (HCs) using the Western Aphasia Battery and neuropsychological test batteries. Moreover, we investigated white matter injury during the acute stage using diffusion magnetic resonance imaging scans for differential tractography. Finally, we used multiple regression models in correlation tractography to analyze the relationship between various language functions and quantitative anisotropy (QA) of WMTs.
RESULTS: Compared with HCs, patients with PSBGA showed lower scores for fluency, comprehension (auditory word recognition and sequential commands), naming (object naming and word fluency), reading comprehension of sentences, Mini-Mental State Examination, and Montreal Cognitive Assessment, along with increased scores in Hamilton Anxiety Scale-17 and Hamilton Depression Scale-17 within 7 days after stroke onset (P < 0.05). Differential tractography revealed that patients with PSBGA had damaged fibers, including in the body fibers of the corpus callosum, left cingulum bundles, left parietal aslant tracts, bilateral superior longitudinal fasciculus II, bilateral thalamic radiation tracts, left fornix, corpus callosum tapetum, and forceps major, compared with HCs (FDR < 0.02). Correlation tractography highlighted that better comprehension was correlated with a higher QA of the left inferior fronto-occipital fasciculus (IFOF), corpus callosum forceps minor, and left extreme capsule (FDR < 0.0083). Naming was positively associated with the QA of the left IFOF, forceps minor, left arcuate fasciculus, and uncinate fasciculus (UF) (FDR < 0.0083). Word fluency of naming was also positively associated with the QA of the forceps minor, left IFOF, and thalamic radiation tracts (FDR < 0.0083). Furthermore, reading was positively correlated with the QA of the forceps minor, left IFOF, and UF (FDR < 0.0083).
CONCLUSIONS: PSBGA is primarily characterized by significantly impaired word fluency of naming and preserved repetition abilities, as well as emotional and cognitive dysfunction. Damaged limbic pathways, dorsally located tracts in the left hemisphere, and left basal ganglia pathways are involved in PSBGA pathogenesis. The results of connectometry analysis further refine the current functional localization model of higher-order neural networks associated with language functions.