Effect of memantine in Alzheimer's disease evaluated by visual-evoked potentials to pattern-reversal, motion-onset, and cognitive stimuli
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- Alzheimerova nemoc farmakoterapie patofyziologie MeSH
- antagonisté excitačních aminokyselin terapeutické užití MeSH
- evokované potenciály účinky léků MeSH
- kognice účinky léků MeSH
- lidé středního věku MeSH
- lidé MeSH
- memantin terapeutické užití MeSH
- neuropsychologické testy MeSH
- pohyb MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- stupeň závažnosti nemoci MeSH
- výsledek terapie MeSH
- zrakové evokované potenciály účinky léků MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antagonisté excitačních aminokyselin MeSH
- memantin MeSH
The authors tested visual-evoked potentials to pattern-reversal, motion-onset, and visual cognitive event-related potentials in 17 patients with mild-to-moderate Alzheimer's disease treated with Memantine (noncompetitive N-methyl-D-aspartic acid antagonist) to verify whether these objective methods can evaluate its therapeutic effect. The patients were examined before Memantine administration and after 3 and 6 months from the treatment onset. Besides electrophysiology, psychologic Alzheimer Disease Assessment Scale-cognitive part (ADAS-cog) test was also performed. Neither ADAS-cog nor any of the electrophysiological tests were able to prove a significant beneficial effect of Memantine therapy in our group of patients. The results of psychologic and electrophysiological tests did not correlate. An individual improvement of ADAS-cog score (decrease of score by 4 and more points) was present in only 29% of patients, improvement of event-related potentials (shortening of P300 peak latency by at least 20 milliseconds) occurred in 42% of patients. Conversely, in 52% of patients, Memantine therapy led to transitory decline of motion processing (delay of N2 peak latency of the motion-onset visual-evoked potentials by at least 10 milliseconds after the first 3 months of therapy, followed by return to pretherapy values in next 3 months).
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