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6594 citation(s) found for "Ha, Richard".

Deep branch ulnar neuropathy due to giant cell tumor
Rafecas, José C., Daube, Jasper R., Ehman, Richard L.

Neurology | May 13, 2012 | Volume: 38 | Issue: 2 | Pages: 327-327

10.1212/wnl.38.2.327 | PMID 3340305 Get It

Stationary waves recorded at the shoulder after median nerve stimulation
Frith, Richard, Benstead, Timothy, Daube, Jasper R.

Neurology | May 13, 2012 | Volume: 36 | Issue: 11 | Pages: 1458-1458

10.1212/wnl.36.11.1458 | PMID 3762965 Get It

Neurologic Munchausen's redux
Folger, W. Neath, Rovner, Richard N., Harter, Donald H., Lipton, Richard B. , Rn, Rovner

Neurology | May 13, 2012 | Volume: 32 | Issue: 2 | Pages: 216

10.1212/wnl.32.2.216-a Get It

Electroencephalographic evaluation in Sturge‐Weber syndrome
Brenner, Richard P., Sharbrough, Frank W.

Neurology | May 13, 2012 | Volume: 26 | Issue: 7 | Pages: 629-629

10.1212/wnl.26.7.629 | PMID 945510 Get It

Spontaneous intracerebellar hemorrhage
Freeman, Richard E., Onofrio, Burton M., Okazaki, Haruo, Dinapoli, Robert P., Freeman, Richard E.

Neurology | May 13, 2012 | Volume: 23 | Issue: 1 | Pages: 84-84

10.1212/wnl.23.1.84 | PMID 4734505 Get It

Neurologic aspects of temporal arteritis
Hollenhorst, Robert W., Brown, Joe R., Wagener, Henry P., Shick, Richard M.

Neurology | May 13, 2012 | Volume: 10 | Issue: 5 | Pages: 490-490

10.1212/wnl.10.5.490 | PMID 14402671 Get It

Ventrolateral and dorsomedial somatosensory association cortex damage produces distinct somesthetic syndromes in humans
Caselli, Richard J.

Neurology | May 13, 2012 | Volume: 43 | Issue: 4 | Pages: 762-762

10.1212/wnl.43.4.762 | PMID 8469337 Get It

Regional cerebral blood flow during acute ischemia Correlation of autoradiographic measurements with observations of cortical microcirculation
Blair, Richard, Waltz, Arthur G.

Neurology | May 13, 2012 | Volume: 20 | Issue: 8 | Pages: 802-802

10.1212/wnl.20.8.802 | PMID 4989333 Get It

Influence of Mitral Regurgitation Repair on Survival in the Surgical Treatment for Ischemic Heart Failure Trial
Grayburn, Paul , Sun, Benjamin , Rao, Vivek , She, Lilin , Jain, Anil, Chua, Yeow Leng , Daly, Richard C. , Senni, Michele , Mokrzycki, Krzysztof , Menicanti, Lorenzo , Oh, Jae K. , Michler, Robert E. , Wróbel, Krzysztof , Lee, Kerry L. , Deja, Marek Andrzej , Krejca, Michał , Lamy, Andre L. , Velazquez, Eric J. , Jones, Robert H. , Senni, Michele

Circulation | May 2, 2012 | Volume: 125 | Issue: 21 | Pages: 2639-2648

10.1161/circulationaha.111.072256 | PMID 22553307 Get It

Background— Whether mitral valve repair during coronary artery bypass grafting (CABG) improves survival in patients with ischemic mitral regurgitation (MR) remains unknown. Methods and Results— Patients with ejection fraction ≤35% and coronary artery disease amenable to CABG were randomized at 99 sites worldwide to medical therapy with or without CABG. The decision to treat the mitral valve during CABG was left to the surgeon. The primary end point was mortality. Of 1212 randomized patients, 435 (36%) had none/trace MR, 554 (46%) had mild MR, 181 (15%) had moderate MR, and 39 (3%) had severe MR. In the medical arm, 70 deaths (32%) occurred in patients with none/trace MR, 114 (44%) in those with mild MR, and 58 (50%) in those with moderate to severe MR. In patients with moderate to severe MR, there were 29 deaths (53%) among 55 patients randomized to CABG who did not receive mitral surgery (hazard ratio versus medical therapy, 1.20; 95% confidence interval, 0.77–1.87) and 21 deaths (43%) among 49 patients who received mitral surgery (hazard ratio versus medical therapy, 0.62; 95% confidence interval, 0.35–1.08). After adjustment for baseline prognostic variables, the hazard ratio for CABG with mitral surgery versus CABG alone was 0.41 (95% confidence interval, 0.22–0.77; P =0.006). Conclusion— Although these observational data suggest that adding mitral valve repair to CABG in patients with left ventricular dysfunction and moderate to severe MR may improve survival compared with CABG alone or medical therapy alone, a prospective randomized trial is necessary to confirm the validity of these observations. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00023595.
Unruptured intracranial aneurysms in the Familial Intracranial Aneurysm and International Study of Unruptured Intracranial Aneurysms cohorts: differences in multiplicity and location
Brown, Robert D., Moomaw, Charles J. , Sauerbeck, Laura, Hornung, Richard, Woo, Daniel, Kleindorfer, Dawn , Flaherty, Matthew L. , Meissner, Irene, Anderson, Craig S. , Connolly, E. Sander , Kallmes, David F. , Torner, James C., Torner, James C. , Mackey, Jason S. , Gandhi, Dheeraj , Rouleau, Guy Armand , Huston, John , Broderick, Joseph P.

Journal of Neurosurgery | April 27, 2012 | Volume: 117 | Issue: 1 | Pages: 60-64

10.3171/2012.4.jns111822 | PMID 22540404 Get It

Object Familial predisposition is a recognized nonmodifiable risk factor for the formation and rupture of intracranial aneurysms (IAs). However, data regarding the characteristics of familial IAs are limited. The authors sought to describe familial IAs more fully, and to compare their characteristics with a large cohort of nonfamilial IAs. Methods The Familial Intracranial Aneurysm (FIA) study is a multicenter international study with the goal of identifying genetic and other risk factors for formation and rupture of IAs in a highly enriched population. The authors compared the FIA study cohort with the International Study of Unruptured Intracranial Aneurysms (ISUIA) cohort with regard to patient demographic data, IA location, and IA multiplicity. To improve comparability, all patients in the ISUIA who had a family history of IAs or subarachnoid hemorrhage were excluded, as well as all patients in both cohorts who had a ruptured IA prior to study entry. Results Of 983 patients enrolled in the FIA study with definite or probable IAs, 511 met the inclusion criteria for this analysis. Of the 4059 patients in the ISUIA study, 983 had a previous IA rupture and 657 of the remainder had a positive family history, leaving 2419 individuals in the analysis. Multiplicity was more common in the FIA patients (35.6% vs 27.9%, p < 0.001). The FIA patients had a higher proportion of IAs located in the middle cerebral artery (28.6% vs 24.9%), whereas ISUIA patients had a higher proportion of posterior communicating artery IAs (13.7% vs 8.2%, p = 0.016). Conclusions Heritable structural vulnerability may account for differences in IA multiplicity and location. Important investigations into the underlying genetic mechanisms of IA formation are ongoing.