Ronald E. Cranford
University of Minnesota
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Neurology | 1978
Ronald E. Cranford; Ilo E. Leppik; Barbara Patrick; Charles B. Anderson; Barbara Kostick
Phenytoin was administered intravenously in large doses (mean = 16.6 mg per kilogram) for prevention and treatment of seizures on 159 occasions to 139 patients aged 17 to 94 years (mean = 52 years) and weighing 37 to 113 kg (mean = 65 kg). Hypotension was more frequent among older patients. No deaths were attributable to phenytoin. Volumes of distribution were relatively constant (mean = 0.78 ± 0.11 liters per kilogram), but half-lives varied considerably and were prolonged (mean = 51 ± 32 hours) because of the large doses administered. A dose of 18 mg per kilogram was effective in maintaining phenytoin serum levels above 10 pg per milliliter for 24 hours.
Neurology | 1979
Ronald E. Cranford; Ilo E. Leppik; Barbara Patrick; Charles B. Anderson; Barbara Kostick
Large doses of phenytoin were administered on 159 occasions to 139 adult patients. Most patients had had more than three seizures or were in status epilepticus. Based on response to treatment, patients could be divided into two groups. Those with excellent response (recurrent seizures, 10%; mortality, 1%) included known epileptics with exacerbation of seizures (n = 79, atypical alcohol withdrawal (61, or miscellaneous conditions (17). Those with poor results (recurrent seizures, 57%; mortality, 38%) included patients with anoxic or metabolic encephalopathy (14), stroke or other vascular disease (14), brain tumor (5), or trauma (5).
Stroke | 1979
David C. Anderson; Ronald E. Cranford
IN THE PATIENT with completed stroke there are few specific management options. Once damage has been sustained, objectives are limited: patient survival, reduction of neurological deficit to a minimum, effective rehabilitation to realize the potential of brain compensatory mechanisms, and secondary prophylaxis in hopes of avoiding a further ictus. The physicians concern must be to minimize the extent of tissue damage incurred as a direct or indirect result of the original vascular process. The record of the many medical interventions which have been advocated with that objective in mind — carbon dioxide inhalation, vasodilating agents, hyperventilation, induced hypertension, and stellate ganglion blockade, to name but a few employed in ischemic infarction — has not been inspiring, and such measures are rarely used today. One intervention, corticosteroid administration, first reported in the late 1950s, however, continues to be routine in many centers. The purpose of our discussion will be to examine, once again, the rationale for the use of corticosteroids in stroke and to assess the evidence that they do, in fact, accomplish the ends for which they are prescribed. Since corticosteroids have been thought to ameliorate the pathological processes in various brain lesions by reducing associated brain edema, we will also consider the nature of ischemic cerebral edema and the evidence that edema contributes to tissue injury.
Neurology | 1998
Ronald E. Cranford
The brain death debate is now 30 years old. Ever since the Harvard Ad Hoc criteria for brain death were published in August 1968, and the proposal was first made that the clinical diagnosis of brain death constituted the legal death of a human being (brain death as death), the brain death controversy has continued.1 However, except for a few unresolved issues, there has been a surprising degree of consensus on the major medical and legal aspects of this subject. One reason for this consensus has been the numerous sets of clinical criteria published by medical, pediatric, neurologic, and neurosurgical organizations in the United States and other countries. Even though these criteria varied somewhat in the clinical features essential to the diagnosis of brain death, the positions of these medical societies strongly supported the view that brain death was a highly reliable diagnosis in most cases.2 In the 1970s, when lawmakers were first involved in enacting statutory legislation equating brain death with death, they were informed by physicians that brain death was a medical syndrome that could be …
The Journal of Medical Humanities | 1981
Ronald E. Cranford; Barbara Patrick
In recent years physicians have used a variety of laboratory studies as confirmatory tests in the diagnosis of brain death. The most widely used test has been the EEG. However, with the development of newer technologies capable of measuring other parameters of brain functions, other laboratory studies are playing an increasingly important role in confirming brain death. In this article, we discuss the role of one of these newer tests, the radioactive brain scan, and compare its advantages and limitations with the EEG.
Neurology | 2002
J. T. Giacino; S. Ashwal; N. Childs; Ronald E. Cranford; B. Jennett; D. I. Katz; J. P. Kelly; J. H. Rosenberg; J. Whyte; R. D. Zafonte; N. D. Zasler; James L. Bernat
JAMA | 2003
Lawrence J. Schneiderman; Todd P. Gilmer; Holly Teetzel; Daniel O. Dugan; Jeffrey Blustein; Ronald E. Cranford; Kathleen B. Briggs; Glen I. Komatsu; Paula Goodman-Crews; Felicia Cohn; Ernlé W. D. Young
Health Affairs | 2005
Todd P. Gilmer; Lawrence J. Schneiderman; Holly Teetzel; Jeffrey Blustein; Kathleen B. Briggs; Felicia Cohn; Ronald E. Cranford; Daniel O. Dugan; Glen I. Komatsu; Ernlé Young
Archive | 2010
Lawrence J. Schneiderman; Todd P. Gilmer; Holly Teetzel; Daniel O. Dugan; Jeffrey Blustein; Ronald E. Cranford; Kathleen B. Briggs; Glen I. Komatsu; Paula Goodman-Crews; Felicia Cohn; Ernlé W. D. Young; Gerald Antoch; Florian M. Vogt; Lutz S. Freudenberg; F. Nazaradeh; Susanne C. Goehde; Jörg Barkhausen; Gerlinde Dahmen; Andreas Bockisch; Joerg F. Debatin; Stefan G. Ruehm; Xh Pang; Zhengge Zhu; F. Xu; Jianhun Guo; X. Gong; David M. Liu; Zhengyu Liu; Daniel P. Chin; D. R. Feikin
Advances in Neurology | 1983
Ilo E. Leppik; Barbara Patrick; Ronald E. Cranford