JavierOlazarán, Fundación Maria Wolff, Montesa 11, E-28006 Madrid, Spainjavier@mariawolff.es
Ruben Muñiz
Submitted March 08, 2005
As Dr. Kavirajan states, our paper has some methodological
limitations which are already discussed in our article. Program attendance and lack of a
dose effect are described in the Results (‘Safety and Compliance’ and last
paragraph) whereas statistical and other limitations regarding study
design are discussed in the final paragraph.
A completely blind assessment in non-pharmacological interventions is
very difficult, if not impossible. Ideally, a mock intervention should
have been designed and implemented but, even under those circumstances, the
quality of blinding is questionable. [3] Kavirajan mentions that
patients and caregivers could have mentioned issues related to cognitive-motor intervention during assessments. It is unlikely that a systematic
bias could have been introduced because our evaluators were blind not
only to patient group, but also to study design.
Since Alzheimer disease (AD) is a progressive and irreversible
condition, lack of deterioration is gaining acceptance as a way of
determining response in long-term trials. [4,5] As long as affective
disturbances increase from mild cognitive impairment to more advanced
dementia stages, defining response should also be adequate for
the affective domain. [6]
The cognitive reserve concept does not predict a poorer
cognitive performance in patients with higher educational attainment.
Rather, cognitive reserve would allow better coping with AD pathology.
For that reason, given a level of clinical severity, the underlying AD
pathology would be more advanced in patients with more cognitive reserve. [7]
These patients would be at their limit of compensating
capacity and therefore would hardly benefit from the strategies given at
the cognitive-motor sessions.
References
3. Davis RN, Massman PJ, Doody RS. Cognitive intervention in
Alzheimer disease: a randomized placebo-controlled study. Alzheimer Dis
Assoc Disord 2001;15:1-9.
4. Farlow M, Anand R, Mesina J, Hartman R, Veach J. A 52-week study
of the efficacy of rivastigmine in patients with mild to moderately severe
Alzheimer’s disease. Eur Neurol 2000; 44: 236-241.
5. Wilcock G, Howe I, Coles H, Lilienfeld S, Truyen L, Zhu Y, et al.
A long-term comparison of galantamine and donepezil in the treatment of
Alzheimer’s disease. Drugs Aging 2003; 20: 777-789.
6. Eastwood R, Reisberg B. Abnormal behaviour in Alzheimer’s disease.
In: Gauthier S, editor. Clinical diagnosis and management of Alzheimer’s
disease. Second edition revised. London: Martin Dunitz 2001; 197-212.
7. Scarmeas N, Stern Y. Cognitive reserve and lifestyle. J Clin Exp
Neuropsychol 2003; 25: 625-633.
As Dr. Kavirajan states, our paper has some methodological limitations which are already discussed in our article. Program attendance and lack of a dose effect are described in the Results (‘Safety and Compliance’ and last paragraph) whereas statistical and other limitations regarding study design are discussed in the final paragraph.
A completely blind assessment in non-pharmacological interventions is very difficult, if not impossible. Ideally, a mock intervention should have been designed and implemented but, even under those circumstances, the quality of blinding is questionable. [3] Kavirajan mentions that patients and caregivers could have mentioned issues related to cognitive-motor intervention during assessments. It is unlikely that a systematic bias could have been introduced because our evaluators were blind not only to patient group, but also to study design.
Since Alzheimer disease (AD) is a progressive and irreversible condition, lack of deterioration is gaining acceptance as a way of determining response in long-term trials. [4,5] As long as affective disturbances increase from mild cognitive impairment to more advanced dementia stages, defining response should also be adequate for the affective domain. [6]
The cognitive reserve concept does not predict a poorer cognitive performance in patients with higher educational attainment. Rather, cognitive reserve would allow better coping with AD pathology. For that reason, given a level of clinical severity, the underlying AD pathology would be more advanced in patients with more cognitive reserve. [7] These patients would be at their limit of compensating capacity and therefore would hardly benefit from the strategies given at the cognitive-motor sessions.
References
3. Davis RN, Massman PJ, Doody RS. Cognitive intervention in Alzheimer disease: a randomized placebo-controlled study. Alzheimer Dis Assoc Disord 2001;15:1-9.
4. Farlow M, Anand R, Mesina J, Hartman R, Veach J. A 52-week study of the efficacy of rivastigmine in patients with mild to moderately severe Alzheimer’s disease. Eur Neurol 2000; 44: 236-241.
5. Wilcock G, Howe I, Coles H, Lilienfeld S, Truyen L, Zhu Y, et al. A long-term comparison of galantamine and donepezil in the treatment of Alzheimer’s disease. Drugs Aging 2003; 20: 777-789.
6. Eastwood R, Reisberg B. Abnormal behaviour in Alzheimer’s disease. In: Gauthier S, editor. Clinical diagnosis and management of Alzheimer’s disease. Second edition revised. London: Martin Dunitz 2001; 197-212.
7. Scarmeas N, Stern Y. Cognitive reserve and lifestyle. J Clin Exp Neuropsychol 2003; 25: 625-633.