|
Mémantine |
mémantine (Ebixa) |
Antagoniste des récepteurs NMDA, assure une neuro-protection par réduction de la neuro-excito-toxicité La mémantine améliore les capacités de mémorisation par facilitation du phénomène de LTP (long terme potential). |
|
![]() |
Synonyms 3,5-Dimethyl-1-adamantanamine hydrochloride |
Modalités de prescriptionMédicament nécessitant une titration Semaine 1 : 1/2 cp le matin Semaine 2 : 1/2 cp le matin et 1/2 cp le soir Semaine 3 : 1 cp le matin, 1/2 cp le soir Semaine 4 : 1 matin et 1 le soir NE JAMAIS ARRETER LES INHINBITEURS DE LA CHOLINESTERASE SOUS PRETEXTE DE L'INTRODUCTION DE L'EBIXA |
|
| Indications | La mémantine a montré une efficacité dans la maladie d'Alzheimer, dans les formes modérées et sévères |
| Efficacité | Retarde le déclin de la perte d'autonomie |
| Effets secondaires | -vertiges -maux de tête -hallucinations |
|
|
| L'entrée toxique du calcium dans les neurones glutamatergiques est bloquée par la mémantine. Ce médicament se fixant sur le récepteur NMDA bloque la porte d'entrée du calcium. | |
|
|
N Engl J Med. 2003 Apr 3;348(14):1333-41.Memantine in moderate-to-severe Alzheimer's disease. Reisberg B, Doody R, Stoffler A, Schmitt F, Ferris S, Mobius HJ; Memantine Study Group. Department of Psychiatry, New York University School of Medicine, New York 10016, USA. barry.reisberg@med.nyu.edu BACKGROUND: Overstimulation of the N-methyl-D-aspartate (NMDA) receptor by glutamate is implicated in neurodegenerative disorders. Accordingly, we investigated memantine, an NMDA antagonist, for the treatment of Alzheimer's disease. METHODS: Patients with moderate-to-severe Alzheimer's disease were randomly assigned to receive placebo or 20 mg of memantine daily for 28 weeks. The primary efficacy variables were the Clinician's Interview-Based Impression of Change Plus Caregiver Input (CIBIC-Plus) and the Alzheimer's Disease Cooperative Study Activities of Daily Living Inventory modified for severe dementia (ADCS-ADLsev). The secondary efficacy end points included the Severe Impairment Battery and other measures of cognition, function, and behavior. Treatment differences between base line and the end point were assessed. Missing observations were imputed by using the most recent previous observation (the last observation carried forward). The results were also analyzed with only the observed values included, without replacing the missing values (observed-cases analysis). RESULTS: Two hundred fifty-two patients (67 percent women; mean age, 76 years) from 32 U.S. centers were enrolled. Of these, 181 (72 percent) completed the study and were evaluated at week 28. Seventy-one patients discontinued treatment prematurely (42 taking placebo and 29 taking memantine). Patients receiving memantine had a better outcome than those receiving placebo, according to the results of the CIBIC-Plus (P=0.06 with the last observation carried forward, P=0.03 for observed cases), the ADCS-ADLsev (P=0.02 with the last observation carried forward, P=0.003 for observed cases), and the Severe Impairment Battery (P<0.001 with the last observation carried forward, P=0.002 for observed cases). Memantine was not associated with a significant frequency of adverse events. CONCLUSIONS: Antiglutamatergic treatment reduced clinical deterioration in moderate-to-severe Alzheimer's disease, a phase associated with distress for patients and burden on caregivers, for which other treatments are not available. Copyright 2003 Massachusetts Medical Society |
|
|