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Background Emergency Medical Services (EMS) is a vital link in the overall chain of stroke survival. A Primary Stroke Center (PSC) relies heavily on the 9-1-1 response system along with the ability of EMS personnel to accurately diagnose acute stroke. Other critical elements include identifying time of symptom onset, providing pre-hospital care, selecting a destination PSC, and communicating estimated time of arrival (ETA). Purpose Our purpose was to evaluate the EMS component of thrombolysed acute ischemic stroke patient care at our PSC. Methods In a retrospective manner we retrieved electronic copies of the EMS incident reports for every thrombolysed ischemic stroke patient treated at our PSC from September 2001 to August 2005. The following data elements were extracted: location of victim, EMS agency, times of dispatch, scene, departure, emergency department (ED) arrival, recordings of time of stroke onset, blood pressure (BP), heart rate (HR), cardiac rhythm, blood glucose (BG), Glasgow Coma Scale (GCS), Cincinnati Stroke Scale (CSS) elements, emergency medical personnel field assessment, and transport decision making. Results Eighty acute ischemic stroke patients received thrombolysis during the study interval. Eighty-one percent arrived by EMS. Two EMS agencies transported to our PSC. Mean dispatch-to-scene time was 6 min, on-scene time was 16 min, transport time was 10 min. Stroke onset time was recorded in 68%, BP, HR, and cardiac rhythm each in 100%, BG in 81%, GCS in 100%, CSS in 100%, and acute stroke diagnosis was made in 88%. Various diagnostic terms were employed: cerebrovascular accident in 40%, unilateral weakness or numbness in 20%, loss of consciousness in 16%, stroke in 8%, other stroke terms in 4%. In 87% of incident reports there was documentation of decision-making to transport to the nearest PSC in conjunction with pre-notification. Conclusion The EMS component of thrombolysed acute ischemic stroke patients care at our PSC appeared to be very good overall. Diagnostic accuracy was excellent, field assessment, decision-making, and transport times were very good. There was still room for improvement in documentation of stroke onset and in employment of a common term for acute stroke.

OBJECTIVE To determine whether migraine with aura and migraine without aura are independent risk factors for symptomatic cardiovascular and cerebrovascular disease. METHODS We addressed the objective through development of a structured critically appraised topic that included a clinical scenario, structured question, search strategy, critical appraisal, results, summary of best evidence, commentary, and bottom-line conclusions. Participants included consultant and resident neurologists, clinical epidemiologists, medical librarians, and clinical content experts. RESULTS A prospective cohort study of 27,840 participants in the Women's Health Study determined that, compared with women lacking a migraine history, women who reported active migraine with aura had adjusted hazard ratios of 2.15 (95% confidence interval [CI], 1.58-2.92) for major cardiovascular disease, 1.91 (95% CI, 1.17-3.10) for ischemic stroke, 1.74 (95% CI, 1.23-2.46) for coronary revascularization, 1.71 (95% CI, 1.16-2.53) for angina, and 2.33 (95% CI, 1.21-4.51) for ischemic cardiovascular disease death. Active migraine without aura was not associated with increased risk of any of the vascular event categories. CONCLUSION In women, active migraine with aura increases the risk of major CVD and ischemic stroke by approximately 2-fold compared with women without migraine. Active migraine without aura was not a risk factor for major CVD and stroke outcomes in this study. Additional emphasis on identification and treatment of modifiable vascular disease risk factors for women with active migraine with aura is warranted.

Although age is a major risk factor for stroke, physicians are often reluctant to use thrombolytic agents in those who are very old. No published study provides detailed information on the use of intravenous tissue plasminogen activator (tPA) in patients aged 90 years or older. We retrospectively reviewed the use of intravenous tPA for patients 90 years or older who were admitted with acute ischemic stroke to the hospital at 4 academic centers from March 1, 1999, to March 1, 2008. We reviewed the clinical features of the patients at presentation, complications, and outcomes. Twenty-two patients (11 women; median age, 93 years; range, 90-101 years) were identified who had received intravenous tPA for symptoms of acute ischemic stroke (average time to treatment, 143 minutes; range, 90-180 minutes; no tPA protocol violations; mean National Institutes of Health Stroke Scale score, 15; range, 5-28). Nearly all patients were highly functional at baseline (median modified Rankin Scale [mRS] score, 1; median Barthel Index score, 95), and all but one performed the activities of daily living with little or no assistance before stroke. By the 30-day follow-up, 2 patients (9%) had a favorable outcome (mRS score, 0-2) and 2 (9%) had moderate disability (mRS score, 3). Most patients died (n=10) or experienced severe disability, defined as an mRS score of 4 or 5 (n=5). Asymptomatic intracerebral hemorrhage occurred in 3 patients (14%) and was nonfatal. Most patients aged 90 years or older who received intravenous tPA for acute ischemic stroke had poor 30-day functional outcomes or died. Intravenous tPA treatment in this age group does not improve the outcome of ischemic stroke.

Two distinct genes encode the 93% homologous type 1 (placenta, peripheral tissues) and type 2 (adrenals, gonads) 3beta-hydroxysteroid dehydrogenase/isomerase (3beta-HSD/isomerase) in humans. Mutagenesis studies using the type 1 enzyme have produced the Y154F and K158Q mutant enzymes in the Y(154)-P-H(156)-S-K(158) motif as well as the Y269S and K273Q mutants from a second motif, Y(269)-T-L-S-K(273), both of which are present in the primary structure of the human type 1 3beta-HSD/isomerase. In addition, the H156Y mutant of the type 1 enzyme has created a chimera of the type 2 enzyme motif (Y(154)-P-Y(156)-S-K(158)) in the type 1 enzyme. The mutant and wild-type enzymes have been expressed and purified. The K(m) value of dehydroepiandrosterone is 13-fold greater, and the maximal turnover rate (K(cat)) is 2-fold greater for wild-type 2 3beta-HSD compared with the wild-type 1 3beta-HSD activity. The H156Y mutant of the type 1 enzyme has substrate kinetic constants for 3beta-HSD activity that are very similar to those of the wild-type 2 enzyme. Dixon analysis shows that epostane inhibits the 3beta-HSD activity of the wild-type 1 enzyme with 14-17-fold greater affinity compared with the wild-type 2 and H156Y enzymes. The Y154F and K158Q mutants exhibit no 3beta-HSD activity, have substantial isomerase activity, and utilize substrate with K(m) values similar to those of wild-type 1 isomerase. The Y269S and K273Q mutants have low, pH-dependent 3beta-HSD activity, exhibit only 5% of the maximal isomerase activity, and utilize the isomerase substrate very poorly. From these studies, a structural basis for the profound differences in the substrate and inhibition kinetics of the wild-type 1 and 2 3beta-HSD, plus a catalytic role for the Tyr(154) and Lys(158) residues in the 3beta-HSD reaction have been identified. These advances in our understanding of the structure/function of human type 1 and 2 3beta-HSD/isomerase may lead to the design of selective inhibitors of the type 1 enzyme not only in placenta to control the onset of labor but also in hormone-sensitive breast, prostate, and choriocarcinoma tumors to slow their growth.

W Oliver Tobin1, Byron R Spencer2, Bart M Demaerschalk21Department of Neurology, Adelaide and Meath Hospital, Dublin, incorporating the National Children’s Hospital, Ireland; 2Department of Neurology, Mayo Clinic Arizona, USAAbstract: Herpes zoster is caused by varicella zoster virus infection involving the dorsal root ganglia of spinal nerve roots. This common problem can be associated with multiple neurological abnormalities. We present a case of Herpes zoster affecting the T1 dermatome associated with ipsilateral Horner’s syndrome and radicular weakness.Keywords: Herpes zoster, Horner’s syndrome, spinal ganglia, postherpetic neuralgia, spinal nerve roots