Ischemic Change

Abstract: Until recently, our understanding of the cellular and subcellular changes evoked by diffuse traumatic brain injury has been framed in the context of primary focal injury. In this regard, the ensuing cell death cascades were linked to contusional-mediated changes associated with frank hemorrhage and ischemia, and these were assumed to contribute to the observed apoptotic and necrotic neuronal death. Little consideration was given to the potential that other non-contusional cell death cascades could have been triggered by the diffuse mechanical forces of injury. While the importance of these classical, contusion-related apoptotic and necrotic cell death cascades cannot be discounted with diffuse injury, more recent information suggests that the mechanical force of injury itself can diffusely porate the neuronal plasmalemma and its axolemmal membranes, evoking other forms of cellular response that can contribute to cell injury or death. In this regard, the duration of the membrane alteration appears to be a dependent factor, with enduring membrane change, potentially leading to irreversible damage, whereas more transient membrane perturbation can be followed by cell membrane resealing associated with recovery and/or adaptive change. With more enduring mechanical membrane perturbation, it appears that some of the traditional death cascades involving the activation of cysteine proteases are at work. Equally important, non-traditional pathways involving the lysosomal dependent release of hydrolytic enzymes may also be players in the ensuing neuronal death. These mechanically related factors that directly impact upon the neuronal somata may also be influenced by concomitant and/or secondary axotomy-mediated responses. This axonal injury, although once thought to involve a singular intraaxonal response to injury, is now known to be more complex, reflecting differential responses to injuries of varying severity. Moreover, it now appears that fiber size and type may also influence the axon's reaction to injury. In sum, this review explicates the complexity of the cellular and subcellular responses evoked by diffuse traumatic brain injury in both the neuronal somata and its axonal appendages. This review further illustrates that our once simplistic views framed by evidence based upon contusional and/or ischemic change do not fully explain the complex repertoire of change evoked by diffuse traumatic brain injury.

Abstract: Intravenous recombinant tissue plasminogen activator (r-tPA) was approved for use in acute ischemic stroke in the United States in 1996. Approximately 2% to 5% of patients with acute ischemic stroke receive r-tPA. Complications related to intravenous r-tPA include symptomatic intracranial hemorrhage, major systemic hemorrhage, and angioedema in approximately 6%, 2%, and 5% of patients, respectively. Risk factors for symptomatic hemorrhage include age, male gender, obesity, increased stroke severity, diabetes, hyperglycemia, uncontrolled hypertension, combination antiplatelet use, large areas of early ischemic change, atrial fibrillation, congestive heart failure, and leukoariosis. A risk factor for angioedema is the use of angiotensin-converting enzyme inhibitor. Risk assessment scores, novel imaging strategies, and telemedicine may offer methods of optimizing the risk–benefit ratio.

Abstract: Background Neurologic complications after cardiac surgery include stroke, encephalopathy, and persistent cognitive impairments. More precise neuroimaging of patients with these complications may lead to a better understanding of the etiology and treatment of these disorders. Objective To study the pattern of ischemic changes on diffusion- and perfusion-weighted magnetic resonance imaging (DWI, and MRPI, respectively) in patients with neurologic complications after cardiac surgery. Methods All records were reviewed of our patients undergoing cardiac surgery in the previous year who also underwent postoperative DWI or MRPI. Neurologic symptoms, vascular studies, and the pattern of ischemic changes were recorded. Acute ischemic lesions were classified as having a territorial, watershed, or lacunar pattern of infarction. Patients with multiple territorial infarcts in differing vascular distributions that were not explained by occlusive vascular lesions were classified as having multiple emboli. Results Fourteen patients underwent DWI and 4 underwent MRPI. Acute infarcts were found in 10 of 14 patients by DWI as compared with 5 of 12 patients by computed tomography. Eight patients presented with encephalopathy (associated with focal neurologic deficits in 4), 4 with focal deficits alone, and 2 with either fluctuating symptoms or transient ischemic attacks. Among patients with encephalopathy, 7 of 8 had patterns of infarction suggestive of multiple emboli, including 3 of 4 patients with no focal neurologic deficits. Several patients had combined watershed and multiple embolic patterns of ischemia. Findings of MRPI studies were abnormal in 2 of 4 patients, showing diffusion-perfusion mismatch; both patients had either fluctuating deficits or transient ischemic attacks, and their conditions improved with blood pressure manipulation. Conclusions In patients with neurologic symptoms after cardiac surgery, DWI is more sensitive to ischemic change than computed tomographic scanning and can demonstrate patterns of infarction that may help us understand etiology. The most common pattern was multiple embolic infarcts. Preliminary experience with MRPI suggests that some patients have persistent diffusion-perfusion mismatch after surgery and may benefit from therapeutic intervention.

Abstract: Background and Purpose— MRI is useful for detecting early ischemic lesions before administration of tissue plasminogen activator in patients with hyperacute ischemic stroke. However, it is unclear whether early ischemic change seen on diffusion-weighted imaging (DWI) can be used to predict patient outcomes. Methods— Consecutive patients with anterior circulation ischemic stroke treated with tissue plasminogen activator within 3 hours of stroke onset were prospectively studied. The National Institutes of Health Stroke Scale score was obtained before and 7 days after tissue plasminogen activator administration. MRI, including DWI, was done before tissue plasminogen activator thrombolysis. The relationship between the DWI Alberta Stroke Programme Early CT Score (ASPECTS) and patients’ outcomes was assessed. Results— The subjects consisted of 49 consecutive patients with stroke (27 males; mean age, 72.9±10.3 years). The median (range) of the baseline DWI ASPECTS value was 9 (3–10). Dramatic improvement was se...