Our data support the safety of administering IV tissue plasminogen activator to patients with suspected acute cerebral ischemia within 3 hours of symptom onset, even when the diagnosis ultimately is found not to be stroke or imaging does not show an infarct.

Acute ischemic stroke patients may benefit from lower head-of-the-bed positions to promote residual blood flow to ischemic brain tissue.

Background and Purpose-We routinely perform an urgent bedside neurovascular ultrasound examination (NVUE) with carotid/vertebral duplex and transcranial Doppler (TCD) in patients with acute cerebral ischemia. We aimed to determine the yield and accuracy of NVUE to identify lesions amenable for interventional treatment (LAITs). Methods-NVUE was performed with portable carotid duplex and TCD using standardized fast-track (Ͻ15 minutes) insonation protocols. Digital subtraction angiography (DSA) was the gold standard for identifying LAIT. These lesions were defined as proximal intra-or extracranial occlusions, near-occlusions, Ն50% stenoses or thrombus in the symptomatic artery.

In order to study the effect of zolmitriptan and rizatriptan in oral sumatriptan nonresponders (defined as lack of response in three or more of five attacks), 56 patients were studied in an open trial in a crossover fashion. Both zolmitriptan, 5 mg, and rizatriptan, 10 mg, were effective in the majority of sumatriptan nonresponders. The response to rizatriptan, 10 mg, appeared to be better than to zolmitriptan, 5 mg. Approximately 19% of sumatriptan nonresponders remained nonresponders to both zolmitriptan and rizatriptan.

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related mortality, but the relative importance of underlying cardiac and respiratory mechanisms remains unclear. To illuminate the interactions between seizures, respiration, cardiac function, and sleep that contribute to SUDEP risk, here we developed a mouse epilepsy monitoring unit (EMU) to simultaneously record video, electroencephalography (EEG), electromyography (EMG), plethysmography, and electrocardiography (ECG) in a commonly used genetic model of SUDEP, the Kcna1 knockout (Kcna1-/-) mouse. During interictal periods, Kcna1-/mice exhibited an abnormal absence of post-sigh apneas and a 3-fold increase in respiratory variability. During spontaneous convulsive seizures, Kcna1-/mice displayed an array of aberrant breathing patterns that always preceded cardiac abnormalities. These findings support respiratory dysfunction as a primary risk factor for susceptibility to deleterious cardiorespiratory sequelae in epilepsy and reveal a new role for Kcna1-encoded Kv1.1 channels in the regulation of basal respiratory physiology.