Acute Ischemic Stroke After Moderate to Severe Traumatic Brain Injury

Abstract

Background and Purpose Traumatic brain injury (TBI) leads to nearly 300 000 annual US hospitalizations and increased lifetime risk of acute ischemic stroke (AIS). Occurrence of AIS immediately after TBI has not been well characterized. We evaluated AIS acutely after TBI and its impact on outcome. Methods A prospective database of moderate to severe TBI survivors, admitted to inpatient rehabilitation at 22 Traumatic Brain Injury Model Systems centers and their referring acute-care hospitals, was analyzed. Outcome measures were AIS incidence, duration of posttraumatic amnesia, Functional Independence Measure, and Disability Rating Scale, at rehabilitation discharge. Results Between October 1, 2007, and March 31, 2015, 6488 patients with TBI were enrolled in the Traumatic Brain Injury Model Systems National Database. One hundred and fifty-nine (2.5%) patients had a concurrent AIS, and among these, median age was 40 years. AIS was associated with intracranial mass effect and carotid or vertebral artery dissection. High-velocity events more commonly caused TBI with dissection. AIS predicted poorer outcome by all measures, accounting for a 13.3-point reduction in Functional Independence Measure total score (95% confidence interval, −16.8 to −9.7; P<0.001), a 1.9-point increase in Disability Rating Scale (95% confidence interval, 1.3–2.5; P<0.001), and an 18.3-day increase in posttraumatic amnesia duration (95% confidence interval, 13.1–23.4; P<0.001). Conclusions Ischemic stroke is observed acutely in 2.5% of moderate to severe TBI survivors and predicts worse functional and cognitive outcome. Half of TBI patients with AIS were aged ≤40 years, and AIS patients more often had cervical dissection. Vigilance for AIS is warranted acutely after TBI, particularly after high-velocity events.

Neuroprotective Effect of Low-Intensity Transcranial Ultrasound Stimulation in Moderate Traumatic Brain Injury Rats

“…There is also a positive correlation between the degree of injury and the severity of complications. Therefore, it is important to research and implement efficient interventions for TBI in order to reduce the abovementioned complications (Scott et al, 2009;Hayes et al, 2017;Kowalski et al, 2017).…”

Does Complement-Mediated Hemostatic Disturbance Occur in Traumatic Brain Injury? A Literature Review and Observational Study Protocol

“…With regards to TBI, there are no studies that have assessed if complement plays a role in the hemostatic disturbance that is seen following injury. Based on the data provided in this review, one might instinctively suggest that any such interaction would result in increased thrombosis, and could thus explain the prothrombotic sate that is seen days to weeks following TBI [53][54][55][56][57]. However, it should be noted that the initial bleeding tendency that is seen following TBI is also believed to be due to unregulated thrombosis, culminating in a consumptive coagulopathy that leads to the exacerbation of hemorrhagic lesions [2].…”

“…Currently, there is controversy within the literature regarding the exact nature of hemostatic perturbations after TBI, and evidence exists for the presence of both a hypercoagulable and hypocoagulable state [2]. For example, while the initial head injury often leads to increased bleeding tendency and the exacerbation of hemorrhagic lesions [2,[46][47][48], TBI is also independently associated with an increased risk for venous thromboembolism [49][50][51][52] and ischemic stroke [53][54][55][56][57]. Autopsy studies have also revealed that micro-thrombosis is present in the majority patients who have died from head trauma [58].…”

Neuroimmunological phenomena involved in chronic traumatic brain injury

“…20 The mechanoporation of the plasmatic membrane leads to an increase in the cell membrane permeability and its subsequent ionic imbalance, which promotes the release of neurotransmitters (due to the entrance of Ca 2+ ) to the synaptic cleft, mainly of glutamate. 20 In parallel, the mechanoporation produced by physical damage and exposure to traumatic events can generate an ischemic brain environment, 21 where the supply of oxygen and glucose to the brain is reduced; 22 a situation that can give way to events influencing cell damage.…”