© 2005 Oxford University Press
CORRESPONDENCE |
RESPONSE: Re: Cancer as a Risk Factor for Dementia: A House Built on Shifting Sand
Affiliation of authors: Department of Neuro-Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX
Correspondence to: Jeffrey S. Wefel, PhD, Department of Neuro-Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Unit 431, Houston, TX 77030 (e-mail: jwefel{at}mdanderson.org).
We commend Heflin et al. for recognizing that the assessment of frank dementia is insufficient and that identification of subtler cognitive dysfunction is of great importance. The comprehensive, interdisciplinary approach utilized to identify and subsequently diagnose cases of frank dementia is also laudable (1). However, using a screening measure to identify subtler cognitive dysfunction remains problematic.
Heflin et al. themselves emphasized that the telephone assessment "was not designed to identify subtle differences in cognitive functioning but to locate individuals whose cognitive function was obviously compromised." From their study data (1), more than 50% of individuals identified as evidencing obvious impairment by telephone screening were not found to have impairment consistent with dementia on formal evaluation. Furthermore, it is well accepted that mental status screening measures are inadequate for assessing and diagnosing subtler cognitive dysfunction (2,3) and may in fact be misleading. For instance, Cullum et al. (4) selected a sample of healthy elderly community-dwelling participants who performed within the average range on a rigorous, standardized, 16-word neuropsychological measure of verbal memory. They subsequently administered three-word memory tests that paralleled the procedure used on the Mini-Mental State Exam (3) and found that approximately 33%–60% of participants recalled zero of three or one of three words. Such studies clearly demonstrate the fallibility of mental status screening approaches when assessing individuals without frank cognitive dysfunction. Thus, we again encourage Heflin et al. to review the test results from the comprehensive neuropsychological evaluations performed on their study sample to determine the incidence of subtler cognitive dysfunction.
If cancer survivors are at increased risk of evidencing cognitive dysfunction, the etiologic rationale provided by Heflin et al. is but one of several competing explanations. In our related editorial (5), we listed several possible mechanisms by which cognitive function may be differentially affected in co-twins with a history of cancer, including the presence of secondary cancers, other organ system damage, the development of other neurologic diseases, or persistent cognitive dysfunction secondary to treatment-related neurotoxicities. Although the presence of impaired cognitive function prior to treatment has been demonstrated for a variety of cancer patients (6,7), we never asserted that any potential differences observed between co-twins with and without a history of cancer were due solely to possible cognitive deficits manifested prior to their cancer treatment.
We agree that information about persistent or late cognitive dysfunction associated with cancer and cancer treatments should be made available to cancer patients and their health care providers. The increased incidence of dementia in co-twins with a history of cancer is interesting and warrants further investigation. We also share the concern of Heflin et al. that cancer patients may suffer from an increased incidence of cognitive dysfunction, although we feel that the etiology and mechanisms still need to be elucidated. Given the importance of this issue and the complex nature of cognitive function, we remain steadfast in our conviction that appropriate methodologic designs using measures appropriate for the measurement of subtler cognitive dysfunction remain critical to provide patients and practitioners with accurate information.
REFERENCES
(1) Gatz M, Fratiglioni, Johansson B, Berg S, Mortimer JA, Reynolds CA, et al. Complete ascertainment of dementia in the Swedish Twin Registry: the HARMONY study. Neurobiol Aging 2005;26:439–47.[CrossRef][Web of Science][Medline]
(2) Meyers CA, Wefel JS. The use of the Mini-Mental State Examination to assess cognitive functioning in cancer trials: No ifs, ands, or buts, or sensitivity. J Clin Oncol 2003;21:3557–8.
(3) Lezak MD. Neuropsychological assessment, 3rd Ed. New York (NY): Oxford University Press; 1995.
(4) Cullum CM, Thompson LL, Smernoff EN. Three-word recall as a measure of memory. J Clin Exp Neuropsychol 1993;15:321–9.[Web of Science][Medline]
(5) Wefel JS, Meyers CA. Cancer as a risk factor for dementia: a house built on shifting sand. J Natl Cancer Inst 2005;97:788–9.
(6) Meyers CA, Byrne KS, Komaki R. Cognitive deficits in patients with small cell lung cancer before and after chemotherapy. Lung Cancer 1995;12:231–5.[CrossRef][Web of Science][Medline]
(7) Wefel JS, Lenzi R, Theriault R, Buzdar AU, Cruickshank S, Meyers CA. "Chemobrain" in breast cancer? A prologue. Cancer 2004;101:466–75.[CrossRef][Web of Science][Medline]
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J Natl Cancer Inst 2005 97: 1550-1551.
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