Absence of Perilesional Neuroplastic Recruitment in Chronic Poststroke Aphasia

失语症 神经可塑性 病变 冲程(发动机) 脑功能偏侧化 医学 中风恢复 心理学 神经科学 听力学 康复 病理 机械工程 工程类
作者
Andrew T. DeMarco,Candace van der Stelt,Sachi Paul,Elizabeth Dvorak,Elizabeth H. Lacey,Sarah F. Snider,Peter E. Turkeltaub
出处
期刊:Neurology [Lippincott Williams & Wilkins]
卷期号:99 (2) 被引量:5
标识
DOI:10.1212/wnl.0000000000200382
摘要

Background and Objectives

A prominent theory proposes that neuroplastic recruitment of perilesional tissue supports aphasia recovery, especially when language-capable cortex is spared by smaller lesions. This theory has rarely been tested directly and findings have been inconclusive. We tested the perilesional plasticity hypothesis using 2 fMRI tasks in 2 groups of patients with previous aphasia diagnosis.

Methods

Two cohorts totaling 82 patients with chronic left-hemisphere stroke with previous aphasia diagnosis and 82 control participants underwent fMRI using either a naming task or a reliable semantic decision task. Individualized perilesional tissue was defined by dilating anatomical lesions and language regions were defined using meta-analyses. Mixed modeling examined differences in activity between groups. Relationships with lesion size and aphasia severity were examined.

Results

Patients exhibited reduced activity in perilesional language tissue relative to controls in both tasks. Although a few cortical regions exhibited greater activity irrespective of distance from the lesion, or only when distant from the lesion, no regions exhibited increased activity only when near the lesion. Larger lesions were associated with reduced language activity irrespective of distance from the lesion. Using the reliable fMRI task, reduced language activity was related to aphasia severity independent of lesion size.

Discussion

We found no evidence for neuroplastic recruitment of perilesional tissue in aphasia beyond its typical role in language. Rather, our findings are consistent with alternative hypotheses that changes in left-hemisphere activation during recovery relate to normalization of language network dysfunction and possibly recruitment of alternate cortical processors. These findings clarify left-hemisphere neuroplastic mechanisms supporting language recovery after stroke.
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