Theory and therapy: ptosis, stasis, and autointoxication.
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Biomedical subjects
Publications and source records attributed to R P Hudson.
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A current hypothesis that the sudden infant death syndrome (SIDS) is a sleep apnea syndrome precipitated by defective control of involuntary respiration prompted the present study in which "reactive gliosis" in sections of the medulla oblongata of 45 SIDS victims was quantitated and compared with that in 20 control infants. Six anatomic regions were studied; five are related and one is unrelated to neural control of involuntary respiration. Increased numbers of "reactive" astrocytes were found in the SIDS group when the counts for all regions were combined (P = .04). Counts were also significantly higher in the SIDS victims for each of three regions alone: (1) the hilum of the inferior olivary nucleus (P = .01); (2) a lateral region (P = .02); and (3) the nucleus of the tractus solitarius (P = .03). The region with the greatest statistical difference, the inferior olivary hilum, has no recognized role in the control of involuntary respiration. There were no consistent associations between reactive astrocyte counts and specific clinical, socioeconomic, and pathologic variables. Characterization of the SIDS group whose counts exceeded that of the highest control infant also did not uncover distinguishing features. This study reinforces previous observations that, at least statistically, an abnormality of the brainstem occurs in a group of SIDS victims in contrast to a group of control infants, but also discloses considerable overlap in the numbers of such cells between these two groups.
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In July 1976 a pneumonialike epidemic from a previously unrecognized microorganism erupted among Legionnaires who had attended a meeting in Philadelphia. There were an estimated 182 cases, in which 29 patients died. Among other things the episodes shows that even in a medically sophisticated industrialized nation, a bacterical pathogen can produce a small epidemic and defy identification for almost 6 months. One historical implication of the event is the need to consider the possibility of a return of large-scale epidemic disease rivaling the sweeps of bubonic plague in fourteenth-century Europe. Such epidemics could occur through any of a variety of microorganismic mechanisms recognized as operating at the present time. It is suggested that humans would react to such a disaster much as their progenitors did centuries ago.
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During the past decade an unprecedented public and professional interest has developed around issues involving death and dying. Persons of differing backgrounds and with different objectives are rushing onto this scene in rapidly increasing numbers. Some of these persons have little understanding of the medical complexities of dying and no clinical experience with dying patients. In this essay I attempt to identify a number of ways in which well-intentioned persons engage dying patients or influence public opinion on death and dying, ways that might prove less than salutary for all concerned.
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A 24-month study of fatalities in North Carolina with high blood ethanol levels (300 mg/100 ml or over) revealed 502 cases with either acute alcoholism or the effects of this range of blood ethanol concentration having caused or contributed to death. This investigation reassessed the criteria for ethanol poisoning, including its cause and manner of death, and revealed recurrent patterns common to this syndrome. This inquiry also contrasted the frequency of ethanol poisoning in different areas of the country.
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