Reporting of critical findings in neuroradiology.

OBJECTIVE: The objective of our study was to assess compliance among academic neuroradiologists in reporting institutionally derived critical findings. MATERIALS AND METHODS: We analyzed 3054 neuroradiology CT and MRI reports generated in 1 month. Reports were categorized by whether or not they contained a critical finding based on a previously established list. The reports were subcategorized by whether the reporting neuroradiologist flagged the report as containing a critical finding and whether the radiologist verbally communicated the critical finding to the referring clinician. Reports were divided into day or night categories and the frequency of critical findings for each time period was calculated. RESULTS: Of the 3054 reports included in this study, 301 (9.9%) had critical findings. Of those 301 reports, 233 (77.4%) were flagged and the referring clinician was called. Of the remaining 68 reports with critical findings, the reporting radiologist did not call the clinician about 35.3% of them (24/68). Of the 2753 reports without critical findings, 2658 (96.5%) were appropriately not flagged and the clinician was not called. However, radiologists called clinicians about 3.5% (95/2753) of the reports without critical findings and erroneously flagged 68.4% (65/95) of those reports as critical. A majority of the cases with critical findings were reported at night (55.1%) despite the fact that 67.2% of the studies occurred during the day. CONCLUSION: Compliance with reporting and communicating critical findings must be monitored. Calling clinicians to report noncritical findings may result in unnecessary interruptions in work flow for radiologists and referring health care providers.

Determination and communication of critical findings in neuroradiology.

PURPOSE: The aims of this study were to analyze reporting of critical findings among neuroradiologists in a university setting and to revise a list of critical findings reflecting an academic clinical practice as part of a practice quality improvement project. MATERIALS AND METHODS: Neuroradiologic studies performed between January 1 and February 28, 2011, containing "critical finding" notations were searched. Reports were matched with an institutionally approved list of critical findings. These findings and unlisted items that were labeled critical were analyzed for frequency, clinical severity, and diagnosis category. The list was revised on the basis of frequency and severity results. RESULTS: A total of 12,607 reports contained 871 critical findings, 608 of which (69.8%) matched the preexisting list. One-third of the findings (263 of 871) labeled critical were not found on the list. Facial, spinal, and calvarial fractures (76 of 263 [28.9%]) and neurovascular injuries (38 of 263 [14.4%]) were the most frequent unlisted findings. A revised list encompassed 86.7% of all communicated neuroradiologic critical findings. CONCLUSIONS: Clinician-approved and neuroradiologist-approved standardized sets of critical findings can facilitate the communication of important results without "overcalling" and decreasing efficiency. Physician judgment of what constitutes a critical finding supersedes any such list, as clinical scenarios are highly variable from patient to patient. Critical findings lists require intermittent revision to reflect practice patterns and changing incidence of disease. Such a review can constitute a practice quality improvement initiative.

GABAergic synaptic inhibition is reduced before seizure onset in a genetic model of cortical malformation.

Malformations of the neocortex are a common cause of human epilepsy; however, the critical issue of how disturbances in cortical organization render neurons epileptogenic remains controversial. The present study addressed this issue by studying inhibitory structure and function before seizure onset in the telencephalic internal structural heterotopia (tish) rat, which is a genetic model of heightened seizure susceptibility associated with a prominent neocortical malformation. Both normally positioned (normotopic) and misplaced (heterotopic) pyramidal neurons in the tish neocortex exhibited lower resting membrane potentials and a tendency toward higher input resistance compared with pyramidal neurons from control brains. GABAergic synaptic transmission was attenuated in the tish cortex, characterized by significant reductions in the frequency of spontaneous IPSCs (sIPSCs) and miniature IPSCs recorded from pyramidal neurons. In addition, the amplitudes of sIPSCs were reduced in the tish neocortex, an effect that was more profound in the normotopic cells. Immunohistochemical assessment of presynaptic GABAergic terminals showed a reduction in terminals surrounding pyramidal cell somata in normotopic and heterotopic tish neocortex. The attenuation of inhibitory innervation was more prominent for normotopic neurons and was associated with a reduction in a subset of GABAergic interneurons expressing the calcium-binding protein parvalbumin. Together, these findings indicate that key facets of inhibitory GABAergic neurotransmission are disturbed before seizure onset in a brain predisposed to developing seizures. Such alterations represent a rational substrate for reduced seizure thresholds associated with certain cortical malformations.

Stability of gene expression in postmortem brain revealed by cDNA gene array analysis.

We utilized nylon arrays to measure gene expression in mouse brains after various postmortem intervals (PMIs). Gene expression after overnight refrigeration or 4 h at room temperature then overnight refrigeration correlated highly and approximately equivalently to that in brains processed immediately. After 8-24 h at room temperature and overnight refrigeration gene expression correlation and equivalency declined, but 90-95% of detected genes were within +/-40% of baseline levels. Brain homogenate pH did not change with PMI.