Allyson R. Zazulia

Background: Technological advances have diminished reliance on classroom attendance for mastering preclinical medical school course content, but nonattendance may have unintended consequence on the learning environment. Perceptions among educators and students regarding the value of attendance and implications of nonattendance have not been systematically studied. Purposes: The purpose of this study was to investigate differences in medical student and faculty attitudes regarding preclinical classroom attendance and the impact of nonattendance on educators and the learning environment. Methods: Using Internet-based surveys, we assessed attitudes about preclinical classroom attendance among medical students and teaching faculty at Washington University School of Medicine. Our primary hypothesis was that students would be less likely than faculty to place societal value on attendance and relate it to professionalism. Results: A total of 382 (79%) of 484 eligible students and 248 (64%) of 387 eligible faculty completed the survey. Both groups recognized a negative impact of poor attendance on faculty enthusiasm for teaching (students 83%, faculty 75%), but faculty were significantly more likely to endorse a negative impact on effectiveness of lectures (75% vs. 42%, p <.0001) and small-groups (92% vs. 76%, p <.0001) and a relationship between attendance and professionalism (88% vs. 68%, p <.0001). Students were significantly more likely to support free choice among learning opportunities (90% vs. 41%, p <.0001) including regularly missing class for research and community service activities (70% vs. 14%, p <.0001) and to consider lecture videos an adequate substitute for attendance (70% vs. 15%, p <.0001). Free-text responses suggested that students tended to view class-going primarily as a tool for learning factual material, whereas many faculty viewed it as serving important functions in the professional socialization process. Conclusions: In this single-center cohort, medical student and teaching faculty attitudes differed regarding the importance of classroom attendance and its relationship to professionalism, findings that were at least partially explained by differing expectations of the purpose of the preclinical classroom experience.

The perihematomal hyperintensity (PHH) is commonly interpreted to represent cerebral edema following intracerebral hemorrhage (ICH), but the accuracy of this interpretation is unknown. We therefore investigated the relationship between the changes in PHH and the changes in hemispheric brain volume as a measure of edema during the first week after ICH.

Studies in transgenic mice overexpressing amyloid precursor protein (APP) demonstrate impaired autoregulation of cerebral blood flow (CBF) to changes in arterial pressure and suggest that cerebrovascular dysfunction may be critically important in the development of pathological Alzheimer's disease (AD). Given the relevance of such a finding for guiding hypertension treatment in the elderly, we assessed autoregulation in individuals with AD. Twenty persons aged 75±6 years with very mild or mild symptomatic AD (Clinical Dementia Rating 0.5 or 1.0) underwent ¹⁵O-positron emission tomography (PET) CBF measurements before and after mean arterial pressure (MAP) was lowered from 107±13 to 92±9 mm Hg with intravenous nicardipine; ¹¹C-PIB-PET imaging and magnetic resonance imaging (MRI) were also obtained. There were no significant differences in mean CBF before and after MAP reduction in the bilateral hemispheres (−0.9±5.2 mL per 100 g per minute, P=0.4, 95% confidence interval (CI)=−3.4 to 1.5), cortical borderzones (−1.9±5.0 mL per 100 g per minute, P=0.10, 95% CI=−4.3 to 0.4), regions of T2W-MRI-defined leukoaraiosis (−0.3±4.4 mL per 100 g per minute, P=0.85, 95% CI=−3.3 to 3.9), or regions of peak ¹¹C-PIB uptake (−2.5±7.7 mL per 100 g per minute, P=0.30, 95% CI=−7.7 to 2.7). The absence of significant change in CBF with a 10 to 15 mm Hg reduction in MAP within the normal autoregulatory range demonstrates that there is neither a generalized nor local defect of autoregulation in AD.

Background and Purpose— Progressive perihematomal cell death over 3 to 4 days has been described after experimental intracerebral hemorrhage (ICH). We investigated whether progressive perihematomal damage occurs in human subjects by measuring relative changes in regional cerebral glucose metabolism with ¹⁸ F-fluorordeoxyglucose (FDG) positron emission tomography at multiple time points during the first week after ICH. Methods— Thirteen subjects with a median hematoma volume of 22 cm ³ were studied 1.0±0.3, 2.9±0.8, and 6.7±1.6 days after ICH. Normalized mean counts in 5 concentric annular 2-mm-thick perihematomal volumes-of-interest (VOIs) were compared to the initial study. Next, automated searches with 0.5 to 5.0 mL spherical VOIs identified maximum focal changes in normalized counts compared to the initial study. Results— No annular or focal decrease in perihematomal FDG uptake developed. Instead, FDG uptake significantly increased at session #2 in the first 3 2-mm annular VOIs (9.2%±14.2, 7.8%±11.3, 5.9%±9.0), returning to baseline at session #3. The VOI search identified focal regions of increased perihematomal FDG uptake relative to the contralateral control hemispheres in 6 subjects, which accounted for the annular increase. Conclusion— Perihematomal glucose metabolism increased transiently in a subset of patients 2 to 4 days after acute ICH. These transient focal increases in glucose metabolism occurring in the brain after acute ICH demonstrate that there are ongoing processes in response to injury that last for days. Although further studies are needed to elucidate their pathophysiology, these processes may be indicative of a prolonged window for intervention to improve neurological outcome.

The regulation of cerebral blood flow (CBF) is complex and influenced by multiple factors, most notably cerebral perfusion pressure (CPP, mean arterial pressure (MAP)-intracranial pressure), partial pressure of carbon dioxide (pCO₂), arterial oxygen content, and cerebral metabolism. The individual relationships between these factors and CBF have been extensively studied. How the factors interrelate and whether perturbations in one influence others is, however, poorly understood. In some disease states such as severe head injury or subarachnoid hemorrhage, regulation to CPP may be abolished yet reactivity to oxygen and CO₂ may be preserved.

Background and Purpose —While the evolution of mass effect after cerebral infarction is well characterized, similar data regarding intracerebral hemorrhage (ICH) are scant. Our goal was to determine the time course and cause for progression of mass effect after ICH. Methods —Patients with spontaneous supratentorial ICH who underwent ≥2 CT scans were identified in our prospectively collected database. CT lesion size and midline shift of the pineal and septum pellucidum were retrospectively measured and correlated with clinical and CT characteristics. Causes for increased midline shift were determined by 2 independent observers. Results —Seventy-six patients underwent 235 scans (3.1±1.3 per patient). Initial CT was obtained within 24 hours of ICH in 66. Twenty-five scans were repeated on day 1, 80 on days 2 through 7, 31 on days 8 through 14, and 24 >14 days after ICH. Midline shift was present on 88% of the initial scans. There were 17 instances of midline shift progression: 10 occurred early (0.2 to 1.7 days) and were associated with hematoma enlargement, and 7 occurred late (9 to 21 days) and were associated with edema progression. Progression of mass effect due to edema occurred with larger hemorrhages ( P Conclusions —Progression of mass effect after ICH occurred at 2 distinct time points: within 2 days, associated with hematoma enlargement, and in the second and third weeks, associated with increase in edema. The clinical significance of later-developing edema is unclear.