Impaired working memory is a common and disabling consequence of traumatic brain injury (TBI) that is caused by aberrant brain processing. However, little is known about the extent to which deficits are perpetuated by specific working memory subprocesses. Using a combined functional magnetic resonance imaging (fMRI) and working memory paradigm, we tested the hypothesis that the pattern of brain activation subserving working memory following TBI would interact with both task demands and specific working memory subcomponents: encoding, maintenance, and retrieval. Forty-three patients with moderate-severe TBI, of whom 25 were in the acute phase of recovery (M = 2.16 months, SD = 1.48 months, range = 0.69 – 6.64 months) and 18 in the chronic phase of recovery (M = 23.44 months, SD = 6.76 months, range = 13.35 – 34.82 months), were compared with 38 demographically similar healthy controls. Behaviourally, we found that working memory deficits were confined to the high cognitive load trials in both acute (P = 0.006) and chronic (P = 0.024) cohorts. Furthermore, results for a subset of the sample (18 chronic TBI and 17 healthy controls) who underwent fMRI revealed that the TBI group showed reduced brain activation when simply averaged across all task trials (regardless of cognitive load or subcomponent). However, interrogation of the subcomponents of working memory revealed a more nuanced pattern of activation. When examined more closely, patterns of brain activity following TBI were found to interact with both task demands and the working memory subcomponent: increased activation was observed during encoding in the left inferior occipital gyrus whereas decreased activation was apparent during maintenance in the bilateral cerebellum and left calcarine sulcus. Taken together, findings indicate an inability to appropriately modulate brain activity according to task demand that is specific to working memory encoding and maintenance.

工作记忆受损是由大脑处理异常引起的创伤性脑损伤 (TBI) 的常见后果。然而，对于特定工作记忆子过程在多大程度上导致缺陷持续存在，人们知之甚少。使用功能性磁共振成像 (fMRI) 和工作记忆范式相结合，我们测试了以下假设：TBI 后促进工作记忆的大脑激活模式会与任务需求和特定工作记忆子组件（编码、维护和检索）相互作用。43 例中重度 TBI 患者，其中 25 例处于急性恢复期（M =  2.16 个月，SD  = 1.48 个月，范围 = 0.69 – 6.64 个月），18 例处于慢性恢复期（M  = 23.44）个月，SD  = 6.76 个月，范围 = 13.35 – 34.82 个月），与 38 名人口统计相似的健康对照进行比较。在行为方面，我们发现工作记忆缺陷仅限于急性（P  = 0.006）和慢性（P  = 0.024）队列的高认知负荷试验。此外，接受 fMRI 的样本子集（18 名慢性 TBI 和 17 名健康对照）的结果显示，当对所有任务试验（无论认知负荷或子成分）进行简单平均时，TBI 组表现出大脑激活减少。然而，对工作记忆子成分的询问揭示了一种更微妙的激活模式。当更仔细地检查时，发现 TBI 后的大脑活动模式与任务需求和工作记忆子成分相互作用：在左枕下回编码期间观察到激活增加，而在双侧小脑和左侧小脑维持期间激活明显减少。距状沟。综上所述，研究结果表明，无法根据特定于工作记忆编码和维护的任务需求适当调节大脑活动。