Abstract
Functional neuroimaging studies in mild traumatic brain injury (mTBI) have been largely limited to patients with persistent post-concussive symptoms, utilizing images obtained months to years after the actual head trauma. We sought to distinguish acute and delayed effects of mild traumatic brain injury on working memory functional brain activation patterns < 72 hours after mild traumatic brain injury (mTBI) and again one-week later. We hypothesized that clinical and fMRI measures of working memory would be abnormal in symptomatic mTBI patients assessed < 72 hours after injury, with most patients showing clinical recovery (i.e., improvement in these measures) within 1 week after the initial assessment. We also hypothesized that increased memory workload at 1 week following injury would expose different cortical activation patterns in mTBI patients with persistent post-concussive symptoms, compared to those with full clinical recovery. We performed a prospective, cohort study of working memory in emergency department patients with isolated head injury and clinical diagnosis of concussion, compared to control subjects (both uninjured volunteers and emergency department patients with extremity injuries and no head trauma). The primary outcome of cognitive recovery was defined as resolution of reported cognitive impairment and quantified by scoring the subject’s reported cognitive post-concussive symptoms at 1 week. Secondary outcomes included additional post-concussive symptoms and neurocognitive testing results. We enrolled 46 subjects: 27 with mild TBI and 19 controls. The time of initial neuroimaging was 48 (+22 S.D.) hours after injury (time 1). At follow up (8.7, + 1.2 S.D., days after injury, time 2), 18 of mTBI subjects (64%) reported moderate to complete cognitive recovery, 8 of whom fully recovered between initial and follow-up imaging. fMRI changes from time 1 to time 2 showed an increase in posterior cingulate activation in the mTBI subjects compared to controls. Increases in activation were greater in those mTBI subjects without cognitive recovery. As workload increased in mTBI subjects, activation increased in cortical regions in the right hemisphere. In summary, we found neuroimaging evidence for working memory deficits during the first week following mild traumatic brain injury. Subjects with persistent cognitive symptoms after mTBI had increased requirement for posterior cingulate activation to complete memory tasks at 1 week following a brain injury. These results provide insight into functional activation patterns during initial recovery from mTBI and expose the regional activation networks that may be involved in working memory deficits.
Highlights
Traumatic Brain Injury (TBI) is a significant medical problem worldwide (e.g., [1]), with as many as 1.7 million people in the US sustaining a head injury each year [2]
Much of the research into task-based brain activation has focused on working memory (WM) tasks, since working memory is one of the domains primarily affected by mild traumatic brain injury (mTBI)
Participants consisted of 27 mild TBI patients, 10 orthopedic controls and 9 healthy controls (Table 1)
Summary
Traumatic Brain Injury (TBI) is a significant medical problem worldwide (e.g., [1]), with as many as 1.7 million people in the US sustaining a head injury each year [2]. The majority (75%) of TBIs are mild (mTBI) [2], and not all individuals who sustain a head injury present to the emergency department While it appears most individuals with mTBI will recover without lengthy post-concussive syndrome, there are currently no known clinical measurements that can predict which patient will experience persistent deleterious outcomes including cognitive (e.g., attention, executive function, memory), emotional (e.g., depression, anxiety, irritability), somatic (e.g., headache, fatigue, dizziness, pain) and physical deficits [4]. Much of the research into task-based brain activation has focused on working memory (WM) tasks, since working memory is one of the domains primarily affected by mTBI This ‘mild’ form of injury induces persisting cognitive dysfunction in approximately 15–20 percent of patients each year, exacting an enormous emotional and financial toll on society [18,19,20,21]. The core regions of the DN include posterior cingulate cortex (PCC)/precuneus, inferior parietal lobule and medial prefrontal/perigenual anterior cingulate (ACC) [33]
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