Section Editor
WriteClick: Editor’s Choice
Robert C. Griggs, MD
Editors’ Note: Mortimer argues that important confounding variables may have biased the conclusion by Alladi et al. on the role of bilingualism in delaying the onset of dementia. Following Mortimer’s comments, Alladi et al. conducted additional analysis of their data to support their conclusion. The attitude of “close enough” is not appropriate when determining brain death. Stadlan comments and supports Frank’s call for action regarding this sensitive issue. —Chafic Karam, MD, and Robert C. Griggs, MD
BILINGUALISM DELAYS AGE AT ONSET OF DEMENTIA, INDEPENDENT OF EDUCATION AND IMMIGRATION STATUS
James A. Mortimer, Tampa, FL: From their study of 648 patients with dementia in a clinic in India, Alladi et al. concluded that bilingualism leads to a delay in onset age of dementia compared with monolingualism.1 The data are not sufficient to draw this conclusion. Age at onset studies conducted in a single disease group cannot indicate associations with risk factors because the age at onset depends on the age distributions of the groups from which the participants are selected in the source population. If monolingual persons die at a younger age on average than their higher-educated bilingual counterparts, then the mean age of monolingual people in the source population will be lower than that of bilingual people. This difference will be reflected in the mean age at onset of any disease of later life, including dementing illnesses. To establish that the finding reflects cognitive reserve and is not an artifact of differing age distributions of monolingual and bilingual people in the source population, the age distribution of the source population by monolingualism/bilingualism needs to be determined. In this study, monolingual patients had a lower education level and greater illiteracy, and they more frequently lived in a rural environment. These factors are known to be related to lower life expectancy. Adjusting for these factors in models restricted to cases cannot address the issue of differences in life expectancy in these groups in the source population. Author Response: Suvarna Alladi, Hyderabad, India; Thomas H. Bak, Tom C. Russ, Edinburgh, UK; Mekala Shailaja, Vasanta Duggirala, Hyderabad, India: Dr. Mortimer raises the important issue of 1936
Neurology 82
May 27, 2014
confounding variables, which are relevant to all observational studies. Our study controlled for these variables1 to a higher degree than others. We succeeded in eliminating the immigration confound. We also examined illiterate monolingual and bilingual participants separately and found an even larger difference than among literate participants. Following Dr. Mortimer’s comments, we conducted an additional analysis, examining rural participants (n 5 149) separately, and still found a difference between monolingual and bilingual participants (56.2 [10.9] vs 60.7 [9.6] years, p , 0.01). Our study was not a single disease study; our cohort comprised different types of dementia with different etiologies, symptomatologies, and, of importance, ages at presentation. If the differences in the age at onset were due to lower life expectancy among monolingual participants, we would expect to find the largest effect in those dementia types that present late. We found the opposite. The largest difference was found in frontotemporal dementia, which presents earlier than other dementias.2 In Alzheimer disease, presenting almost a decade later, the difference was smaller, and in dementia with Lewy bodies and mixed dementia— the highest age at presentation—the difference was the smallest. Future studies should further minimize potential confounding variables and this will better clarify these associations. © 2014 American Academy of Neurology 1.
2.
Alladi S, Bak TH, Duggirala V, et al. Bilingualism delays age at onset of dementia, independent of education and immigration status. Neurology 2013;81:1938–1944. Ratnavalli E, Brayne C, Dawson K, Hodges JR. The prevalence of frontotemporal dementia. Neurology 2002;58: 1615–1621.
PRACTICE VARIABILITY IN BRAIN DEATH DETERMINATION: A CALL TO ACTION
Noam Y. Stadlan, Skokie, IL: Shappell et al.1 highlighted the problems concerning determinations of death. If documentation reflects reality, some patients were declared dead with neither an apnea test nor confirmatory testing. The attitude of “close enough” is not appropriate. The neurologic/neurosurgical community must ensure that determinations of death are properly done. Ancillary testing can ideally be
based on the underlying pathology. If further examination is done because an apnea test is not possible, examinations need to confirm that the brainstem is not functioning. An EEG is not certain in that regard. Nuclear medicine testing with nonlipophilic tracers lacks the needed sensitivity. Transcranial Doppler (TCD) showing no flow in the middle cerebral artery does not preclude brainstem function. Finally, a breathing and posturing patient has been reported with reversal of diastolic flow on TCD in the basilar artery,2 which casts doubt on the predictive value of that finding in the posterior circulation. Outside of these caveats, the finding of cerebral circulatory arrest on an adequate study is predictive of loss of brainstem function and consciousness. Due to possible clinical inaccuracies, cerebral blood flow studies should be done routinely. In cases of primary brainstem pathology, EEGs should also be performed. Author Response: Jeffrey I. Frank, Chicago: We thank Dr. Stadlan for his comments. We agree that “close enough” is not appropriate for brain death determination and appreciate his support for our call to action. We also applaud his comments regarding
the idea that ancillary tests, when employed, must be tailored to the mechanism of brain injury to properly support brain death determination in specific circumstances. While this can be better supported by more prescriptive guidelines, clarification of ideal techniques, and objective and contextual interpretation of test results, it is most important that physicians fully understand brain death when approaching its determination. It is this deep understanding that guides a coherent approach to brain death determination and is necessary for the proper application of even the most well-crafted guidelines. Again, this supports our call to action to raise the bar through improved uniformity of policies, physician education, and, in the future, a version of credentialing. © 2014 American Academy of Neurology 1.
2.
Shappell CN, Frank JI, Husari K, Sanchez M, Goldenberg F, Ardelt A. Practice variability in brain death determination: a call to action. Neurology 2013;81: 2009–2014. Budohoski KP, Aries MJH, Kirkpatrick PJ, Lavinio A. Protracted cerebral circulatory arrest and cortical electrical silence coexisting with preserved respiratory drive and flexor motor response. Br J Anaesth 2012;109:293–294.
WriteClick: Rapid Online Correspondence The editors encourage comments about recent articles through WriteClick: Go to www.neurology.org and click on the “WriteClick” tab at the top of the page. Responses will be posted within 72 hours of submission. Before using WriteClick, remember the following:
• WriteClick is restricted to comments about studies published in Neurology within the last eight weeks • Read previously posted comments; redundant comments will not be posted • Your submission must be 200 words or less and have a maximum of five references; reference one must be the article on which you are commenting • You can include a maximum of five authors (including yourself)
Author disclosures are available upon request ([email protected]). Neurology 82
May 27, 2014
1937
Practice variability in brain death determination: A call to action Noam Y. Stadlan and Jeffrey I. Frank Neurology 2014;82;1936-1937 DOI 10.1212/01.wnl.0000450702.68005.e9 This information is current as of May 26, 2014 Updated Information & Services
including high resolution figures, can be found at: http://www.neurology.org/content/82/21/1936.2.full.html
References
This article cites 2 articles, 2 of which you can access for free at: http://www.neurology.org/content/82/21/1936.2.full.html##ref-list-1
Permissions & Licensing
Information about reproducing this article in parts (figures,tables) or in its entirety can be found online at: http://www.neurology.org/misc/about.xhtml#permissions
Reprints
Information about ordering reprints can be found online: http://www.neurology.org/misc/addir.xhtml#reprintsus
Neurology ® is the official journal of the American Academy of Neurology. Published continuously since 1951, it is now a weekly with 48 issues per year. Copyright © 2014 American Academy of Neurology. All rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X.
WriteClick: Editor’s Choice
Robert C. Griggs, MD
Editors’ Note: Mortimer argues that important confounding variables may have biased the conclusion by Alladi et al. on the role of bilingualism in delaying the onset of dementia. Following Mortimer’s comments, Alladi et al. conducted additional analysis of their data to support their conclusion. The attitude of “close enough” is not appropriate when determining brain death. Stadlan comments and supports Frank’s call for action regarding this sensitive issue. —Chafic Karam, MD, and Robert C. Griggs, MD
BILINGUALISM DELAYS AGE AT ONSET OF DEMENTIA, INDEPENDENT OF EDUCATION AND IMMIGRATION STATUS
James A. Mortimer, Tampa, FL: From their study of 648 patients with dementia in a clinic in India, Alladi et al. concluded that bilingualism leads to a delay in onset age of dementia compared with monolingualism.1 The data are not sufficient to draw this conclusion. Age at onset studies conducted in a single disease group cannot indicate associations with risk factors because the age at onset depends on the age distributions of the groups from which the participants are selected in the source population. If monolingual persons die at a younger age on average than their higher-educated bilingual counterparts, then the mean age of monolingual people in the source population will be lower than that of bilingual people. This difference will be reflected in the mean age at onset of any disease of later life, including dementing illnesses. To establish that the finding reflects cognitive reserve and is not an artifact of differing age distributions of monolingual and bilingual people in the source population, the age distribution of the source population by monolingualism/bilingualism needs to be determined. In this study, monolingual patients had a lower education level and greater illiteracy, and they more frequently lived in a rural environment. These factors are known to be related to lower life expectancy. Adjusting for these factors in models restricted to cases cannot address the issue of differences in life expectancy in these groups in the source population. Author Response: Suvarna Alladi, Hyderabad, India; Thomas H. Bak, Tom C. Russ, Edinburgh, UK; Mekala Shailaja, Vasanta Duggirala, Hyderabad, India: Dr. Mortimer raises the important issue of 1936
Neurology 82
May 27, 2014
confounding variables, which are relevant to all observational studies. Our study controlled for these variables1 to a higher degree than others. We succeeded in eliminating the immigration confound. We also examined illiterate monolingual and bilingual participants separately and found an even larger difference than among literate participants. Following Dr. Mortimer’s comments, we conducted an additional analysis, examining rural participants (n 5 149) separately, and still found a difference between monolingual and bilingual participants (56.2 [10.9] vs 60.7 [9.6] years, p , 0.01). Our study was not a single disease study; our cohort comprised different types of dementia with different etiologies, symptomatologies, and, of importance, ages at presentation. If the differences in the age at onset were due to lower life expectancy among monolingual participants, we would expect to find the largest effect in those dementia types that present late. We found the opposite. The largest difference was found in frontotemporal dementia, which presents earlier than other dementias.2 In Alzheimer disease, presenting almost a decade later, the difference was smaller, and in dementia with Lewy bodies and mixed dementia— the highest age at presentation—the difference was the smallest. Future studies should further minimize potential confounding variables and this will better clarify these associations. © 2014 American Academy of Neurology 1.
2.
Alladi S, Bak TH, Duggirala V, et al. Bilingualism delays age at onset of dementia, independent of education and immigration status. Neurology 2013;81:1938–1944. Ratnavalli E, Brayne C, Dawson K, Hodges JR. The prevalence of frontotemporal dementia. Neurology 2002;58: 1615–1621.
PRACTICE VARIABILITY IN BRAIN DEATH DETERMINATION: A CALL TO ACTION
Noam Y. Stadlan, Skokie, IL: Shappell et al.1 highlighted the problems concerning determinations of death. If documentation reflects reality, some patients were declared dead with neither an apnea test nor confirmatory testing. The attitude of “close enough” is not appropriate. The neurologic/neurosurgical community must ensure that determinations of death are properly done. Ancillary testing can ideally be
based on the underlying pathology. If further examination is done because an apnea test is not possible, examinations need to confirm that the brainstem is not functioning. An EEG is not certain in that regard. Nuclear medicine testing with nonlipophilic tracers lacks the needed sensitivity. Transcranial Doppler (TCD) showing no flow in the middle cerebral artery does not preclude brainstem function. Finally, a breathing and posturing patient has been reported with reversal of diastolic flow on TCD in the basilar artery,2 which casts doubt on the predictive value of that finding in the posterior circulation. Outside of these caveats, the finding of cerebral circulatory arrest on an adequate study is predictive of loss of brainstem function and consciousness. Due to possible clinical inaccuracies, cerebral blood flow studies should be done routinely. In cases of primary brainstem pathology, EEGs should also be performed. Author Response: Jeffrey I. Frank, Chicago: We thank Dr. Stadlan for his comments. We agree that “close enough” is not appropriate for brain death determination and appreciate his support for our call to action. We also applaud his comments regarding
the idea that ancillary tests, when employed, must be tailored to the mechanism of brain injury to properly support brain death determination in specific circumstances. While this can be better supported by more prescriptive guidelines, clarification of ideal techniques, and objective and contextual interpretation of test results, it is most important that physicians fully understand brain death when approaching its determination. It is this deep understanding that guides a coherent approach to brain death determination and is necessary for the proper application of even the most well-crafted guidelines. Again, this supports our call to action to raise the bar through improved uniformity of policies, physician education, and, in the future, a version of credentialing. © 2014 American Academy of Neurology 1.
2.
Shappell CN, Frank JI, Husari K, Sanchez M, Goldenberg F, Ardelt A. Practice variability in brain death determination: a call to action. Neurology 2013;81: 2009–2014. Budohoski KP, Aries MJH, Kirkpatrick PJ, Lavinio A. Protracted cerebral circulatory arrest and cortical electrical silence coexisting with preserved respiratory drive and flexor motor response. Br J Anaesth 2012;109:293–294.
WriteClick: Rapid Online Correspondence The editors encourage comments about recent articles through WriteClick: Go to www.neurology.org and click on the “WriteClick” tab at the top of the page. Responses will be posted within 72 hours of submission. Before using WriteClick, remember the following:
• WriteClick is restricted to comments about studies published in Neurology within the last eight weeks • Read previously posted comments; redundant comments will not be posted • Your submission must be 200 words or less and have a maximum of five references; reference one must be the article on which you are commenting • You can include a maximum of five authors (including yourself)
Author disclosures are available upon request ([email protected]). Neurology 82
May 27, 2014
1937
Practice variability in brain death determination: A call to action Noam Y. Stadlan and Jeffrey I. Frank Neurology 2014;82;1936-1937 DOI 10.1212/01.wnl.0000450702.68005.e9 This information is current as of May 26, 2014 Updated Information & Services
including high resolution figures, can be found at: http://www.neurology.org/content/82/21/1936.2.full.html
References
This article cites 2 articles, 2 of which you can access for free at: http://www.neurology.org/content/82/21/1936.2.full.html##ref-list-1
Permissions & Licensing
Information about reproducing this article in parts (figures,tables) or in its entirety can be found online at: http://www.neurology.org/misc/about.xhtml#permissions
Reprints
Information about ordering reprints can be found online: http://www.neurology.org/misc/addir.xhtml#reprintsus
Neurology ® is the official journal of the American Academy of Neurology. Published continuously since 1951, it is now a weekly with 48 issues per year. Copyright © 2014 American Academy of Neurology. All rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X.
