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ARTICLES: David L. Nyenhuis, Philip B. Gorelick, Sally Freels, and David C. Garron Cognitive and functional decline in African Americans with VaD, AD, and stroke without dementia Neurology 2002; 58: 56-61 [Abstract] [Full text] [PDF]

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Reply to Letter to the Editor

David L. Nyenhuis, Philip B. Gorelick   (29 April 2002)

Cognitive and functional decline in African Americans with VaD, AD, and stroke without

Anna M Barrett   (29 April 2002)

Reply to Letter to the Editor 29 April 2002
David L. Nyenhuis Rush-Presbyterian-St. Luke's Medical Center, Philip B. Gorelick Send Correspondence to journal: Re: Reply to Letter to the Editor dnyenhui{at}rush.edu David L. Nyenhuis, et al.	We thank Dr. Barrett for her interest and questions regarding our study [1]. The study's purpose was to compare and describe the cognitive and functional decline of African American patients diagnosed at baseline with Alzheimer's disease, vascular dementia or stroke without dementia. The study was observational. The medical treatment of the patients enrolled in the study was not affected by their participation. We have examined the effects of medications prescribed by the subject's physicians during the study. The results of these analyses are currently under review. We agree with Dr. Barrett that more research needs to be completed to investigate possible treatments for AD and VaD in African American patients. The Center for Stroke Research at Rush-Presbyterian- St. Luke's Medical Center is currently completing a nationwide, multi- site, clinical trial comparison of aspirin and ticlopidine in the prevention of recurrent stroke in over 1800 African Americans [2,3, 4]. Dr. Barrett also inquired about the effects of lesion location in our three groups. We have previously published a study examining this [5]. Our CT data showed that the presence of white matter lesions, nonlacunar infarcts, and left subcortical infarcts were predictors of VaD when compared with AD, whereas atrophy of the third ventricle and equal distribution of white matter lesions distinguished VaD from SWD. On MRI, atrophy of the temporal sulci, temporal horns, and the third ventricle, as well as right hemisphere infarcts, distinguished AD from VaD, while atrophy of the third ventricle differentiated VaD from SWD. The CT and MRI findings among our African American patients were similar to those reported in other dementia studies. References: 1. Nyenhuis DL, Gorelick POB, Freels S, et al. Cognitive and functional decline in African Americans with VaD, AD, and stroke without dementia. Neurology 2002;58: 56-61. 2. Gorelick PB, Leurgans SL, Richardson D, Harris Y, Billingsley M. African American Antiplatelet Stroke Prevention Study (AAASPS): Clinical trial design. J Stroke Cerebrovasc Dis 1998;7:426-434. 3. Gorelick PB. Cerebrovascular disease in African Americans. Stroke 1998;29:2656-2664. 4. Harris Y, Gorelick PB, Samuels, P, Bempong I. Why African Americans may not be participating in clinical trials. J Natl Med Assoc 1996;88:630-634. 5. Charletta D, Gorelick PB, Dollear TJ, Freels S, Harris Y. CT and MRI findings among African Americans with Alzheimer's disease, vascular dementia, and stroke without dementia. Neurology 1995;45:1456-1461.
Cognitive and functional decline in African Americans with VaD, AD, and stroke without 29 April 2002
Anna M Barrett Pennsylvania State University College of Medicine Hershey PA Send Correspondence to journal: Re: Cognitive and functional decline in African Americans with VaD, AD, and stroke without ambarrett{at}psu.edu Anna M Barrett	I read with interest the article by Nyenhuis et al. [1] on progression of vascular dementia versus neurodegenerative dementia of the Alzheimer type. The authors' state the examining effects of the treatments that demented subjects receive, and the areas of the brain affected by ischemia, was beyond the scope of their article. However, if readers have some general information about these factors, they can more appropriately generalize the reported results. Slowing the course of decline has been a focus of research on dementia therapies. Currently, Caucasian patients with AD may receive Vitamin E and a cholinesterase-inhibitor. Caucasian VaD patients may be aggressively monitored for BP and DM control, and given a neuroprotective or nootropic medication [2,3]. Were the African American patients candidates for these or other treatments? Certain brain areas are felt to critically support certain cognitive functions. This would imply that some strokes (e.g., left MCA, thalamocortical white matter) might increase risk of dementia more than others [4,5]. Can the authors provide some data about the location of strokes in SWD subjects, before we incorrectly generalize these results to other patients not demented after stroke? References: 1. Nyenhuis DL, Gorelick POB, Freels S, et al. Cognitive and functional decline in African Americans with VaD, AD, and stroke without dementia. Neurology 2002;58: 56-61. 2. Anonymous. European Pentoxifylline Multi-Infarct Dementia Study. Eur Neurol 1996;36:315-321. 3. Roman G. Perspectives in the treatment of vascular dementia. Drugs Today 2000; 39: 641-653. 4. Tatemichi TK. Desmond DW. Prohovnik I et al.. Confusion and memory loss from capsular genu infarction: a thalamocortical disconnection syndrome? Neurology 1992;42:1966-1979. 5. Tatemichi TK, Desmond DW, Paik M et al. Clinical determinants of dementia related to stroke. Ann Neurol 1993;33: 568-575.