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.

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• Superior mesenteric artery (SMA) stenosis is often responsible for ischaemic symptoms. • Treatment with percutaneous transluminal angioplasty (PTA) seems superior to stenting • Although technical success rates are improved with the use of stents. • Higher mortality in the elderly and those presenting with nausea/vomiting/bloody stools.

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.

BACKGROUND AND PURPOSE The Joint Commission has identified timely reporting of critical results as one of the National Patient Safety Goals. We surveyed directors of neuroradiology fellowships to assess and compare critical findings lists across programs. MATERIALS AND METHODS A 3-question survey was e-mailed to directors of neuroradiology fellowships with the following questions: 1) Do you currently have a “critical findings” list that you abide by in your neuroradiology division? 2) How is that list distributed to your residents and fellows for implementation, if at all? and 3) Was this list vetted by neurology, neurosurgery, and otolaryngology departments? Programs with CF lists were asked for a copy of the list. Summary and comparative statistics were calculated. RESULTS Fifty-one of 89 (57.3%) programs responded. Twenty-one of 51 (41.2%) programs had CF lists. Lists were distributed during orientation, sent via Web sites and e-mails, and posted in work areas. Eleven of 21 lists were developed internally, and 5 of 21, with the input from other departments. The origin of 5 of 21 lists was unknown. Forty CF entities were seen in 20 submitted lists (mean, 9.1; range, 2–23). The most frequent entities were the following: cerebral hemorrhage (18 of 20 lists), acute stroke (15 of 20), spinal cord compression (15 of 20), brain herniation (12 of 20), and spinal fracture/instability (12 of 20). Programs with no CF lists called clinicians on the basis of “common sense” and “clinical judgment.” CONCLUSIONS Less than a half (41.2%) of directors of neuroradiology fellowships that responded have implemented CF lists. CF lists have variable length and content and are predominantly developed by radiology departments without external input.