No abstract available.
Memantine

OBJECTIVE: This study examined the efficacy and safety of memantine-an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist-in the treatment of moderate-to-severe dementia. METHODS: Forty-four patients with moderate-to-severe dementia received 20 mg of memantine daily for 24 weeks. The primary efficacy variable was measured by the Korean version of Severe Impairment Battery(K-SIB), and the secondary efficacy variables were measured using the Seoul-Activites of Daily Living(S-ADL) and Neuropsychiatric Inventory-Questionnaire(NPI-Q). Neuropsychological assessments were administrated at baseline, 12 weeks, and 24 weeks. Safety parameters were monitored. RESULTS: Of 44 patients recruited, 30 completed the study and 14 dropped out. Memantine-treated patients showed a therapeutic benefit in all efficacy variables ; the K-SIB, S-ADL, and NPI-Q total scores were not significantly different from baseline either at the endpoint(in the analysis of intention-to-treat, with the last observation carried forward, ITT-LOCF) or at week 24(in the analysis of observed cases, OC). The response rates, when "response" was defined as improved or unchanged in the K-SIB or the S-ADL scores, were 43.3 and 50%, respectively(in the analysis of OC). The responders showed significant improvement in the cognitive subdomain of memory function, praxis, visuospatial ability, and orienting to name. Memantine was shown to be tolerable and safe. CONCLUSIONS: Memantine treatment reduced or delayed clinical deterioration in cognition, function, and behavior in patients with moderate-to-severe dementia.
Cognition ; Dementia* ; Humans ; Memantine* ; Memory ; N-Methylaspartate

This case report highlights the challenges in managing Frontal Lobe Syndrome (FLS) in a patient with end-stage renal disease. Methods: This is a case description of a 58 year-old gentleman who presented with behavioural changes: irritability, mood lability, aggression, psychosis, and overfamiliarity. His presenting symptoms were in keeping with (FLS) with positive findings on Computed Tomography (CT) scan of the brain and also neuropsychological assessments. Difficulties arose in attempts to control his aggression without further compromising his renal function. Results: The usage of the commonly used antipsychotics in controlling aggression was restricted in view of the patient’s renal impairment. Augmentation with low dose memantine proved to be beneficial in this case, without causing further deterioration in renal function. Conclusion: The use of memantine to augment the effect of risperidone was observed to be safe and successful in managing the behavioural changes associated with FLS in adults with end-stage renal disease.
Frontal Lobe ; Memantine ; Kidney Failure, Chronic

Introduction. Migraine is a common, debilitating primary headache. Memantine is a non-competitive N-methyl D-aspartate (NMDA) antagonist that lowers neuronal excitability that could prevent migraine attacks. This study aimed to determine the efficacy and safety of memantine in patients with episodic migraine attacks using a systematic review and meta-analysis.

Methods. We searched CENTRAL, MEDLINE, Scopus, Cochrane, LILACS, ClinicalTrials.gov, HERDIN and Google Scholar for relevant studies until July 31, 2020. Prespecified screening and eligibility criteria for inclusion were applied. Included studies underwent methodological quality assessment. Study design, patient characteristics, interventions given, and relevant outcomes were extracted and synthesized.

Results. This review included five relevant articles - two randomized controlled trials (RCT) and three non randomized studies (one retrospective records review and survey, two prospective open-label single-arm trials). There were 109 patients included in the RCTs and 197 patients reported in the non-randomized studies. Pooled data from the two RCTs showed that memantine at 10 mg/day significantly decreased the monthly number of migraine days at 12 weeks compared to placebo with a mean difference of -1.58 [95% confidence interval (CI) -1.84, -1.32]. Non-randomized studies also showed a decrease in migraine days per month with memantine (5 to 20 mg/day) after 12 weeks [95% CI]: -9.1 [-11, -7.23], -7.2 [-8.85, -5.55], and -4.9 [-6.29, -3.51]. Adverse drug events (ADE) did not differ significantly between patients treated with memantine compared to placebo.

Conclusion. Memantine may be effective and well-tolerated as prophylaxis for episodic migraine.

The objective of this study was to determine the effect of memantine on schizophrenia-like symptoms in a ketamine-induced social withdrawal model in rats. We examined therapeutic effects of memantine, an NMDA antagonist, and haloperidol, a classic antipsychotic drug, on this behavioral model. Administration of memantine (10 or 15 mg.kg(-1)) significantly reduced ketamine-induced social withdrawal, and this effect was more effective than that of haloperidol (0.25 mg.kg(-1)) by restoring the social interaction between rats with no modification in general motor activity. These results suggest that memantine could have a therapeutic potential for schizophrenia.
Animals ; Haloperidol ; Interpersonal Relations ; Ketamine ; Memantine ; Motor Activity ; N-Methylaspartate ; Rats ; Schizophrenia

OBJECTIVE: To investigate the effects of memantine, an N-methyl-d-aspartate (NMDA) receptor antagonist, on cognitive impairments in patients with chronic schizophrenia. METHODS: A 12-week, placebo-controlled trial was conducted to determine the effectiveness of memantine as an adjunctive treatment with conventional antipsychotic medications in 26 patients with chronic schizophrenia. The subjects were evaluated with the Korean version of the Mini-Mental State Examination (K-MMSE), the Positive and Negative Syndrome Scale (PANSS), the Hamilton Rating Scale for Depression (HAM-D), and a standard neuropsychological screening test. RESULTS: Memantine treatment was not associated with significantly improved cognitive test scores compared with the placebo control treatment. An improvement in the scores on the PANSS negative subscale was noted with memantine, but it was not significant. CONCLUSION: Adjunctive memantine treatment did not improve cognitive functioning or affect psychopathology in patients with chronic schizophrenia in the present study. Memantine, however, was tolerated well and did not exacerbate positive symptoms in patients with chronic schizophrenia.
Antipsychotic Agents ; Cognition ; Depression ; Humans ; Mass Screening ; Memantine ; N-Methylaspartate ; Pilot Projects ; Psychopathology ; Schizophrenia

Alcohol-induced cognitive disorder is a very severe problem in problem alcohol drinker and alcohol itself seems to be one of the main causalities in the development of senile dementia. However, the spectrum of alcohol induced cognitive disorder is quite broad, for example, it covered from alcohol-induced persistent amnestic disorder to Wernicke-Korsakoff syndrome and alcohol-induced persistent dementia. By that reason, broad spectrum of cognitive impairment by excessive alcohol drinking is regarded as alcohol related dementia. The pharmacological treatment is not well established yet in alcohol related dementia, except Wernicke-Korsakoff syndrome which is definitely related to thiamine deficiency. Therefore we introduced that some reports about the clinical efficacies by rivastigmine or donepezil trial and recent outcomes of memantine trial by authors in this review.
Alcohol Drinking ; Alzheimer Disease ; Dementia ; Indans ; Korsakoff Syndrome ; Memantine ; Phenylcarbamates ; Piperidines ; Rivastigmine ; Thiamine ; Thiamine Deficiency

The pharmacological treatment of Alzheimer's disease is based on symptomatic therapy of cognitive decline and behavioral problems. Numerous therapies have been investigated for the treatment and prevention of Alzheimer's disease. We reviewed the current evidence-based medical research and guidelines of treatment for Alzheimer's disease. The use of cholinesterase inhibitors (ChEI) and N-methyl-D-aspartate (NMDA) inhibitors can bring about significant but modest therapeutic improvement. There is insufficient evidence to recommend vitamine E, estrogen, ginko biloba, or nonsteroidal anti-inflammatory drugs (NSAIDs) for the prevention or treatment of Alzheimer's disease. This article reviews the available data on current pharmacological treatments through evidence-based medicine.
Alzheimer Disease ; Cholinesterase Inhibitors ; Estrogens ; Evidence-Based Medicine ; Ginkgo biloba ; Memantine ; N-Methylaspartate ; Vitamins

Alcohol-related problems are prevalent and lead to substantial economic, physical, and psychological burden. Among the various effects of alcohol, the effect on the brain is a matter of importance. The brain controls drinking behaviors and may be damaged earlier than other organs by alcohol. Moreover, alcohol-related brain pathologies are difficult to treat once they have progressed. Therefore, we overviewed the mechanisms and results of alcohol-induced brain damage and interventions against it in this article. Alcohol exerts neurotoxic effects mediated by various mechanisms, such as acetaldehyde toxicity, glutamate excitotoxicity, increased oxidative stress, and chronic inflammatory responses. In both functional and structural neuroimaging studies, the evidence of alcohol-induced brain damage was observed in various regions of gray and white matter. Brain damage has been known to be more prominent when it begins during the period of brain development and in women. Symptomatically, alcohol hangovers and alcohol-induced blackouts, which are highly prevalent alcohol-related problems, have been suggested to be early signs of alcohol-related brain damage. However, neurological changes induced by alcohol have been reported to be partly recovered by abstinence. The development of effective interventions would be clinically important. Although following the rules of low-risk drinking and abstinence have been the primary approaches up to the present, studies on mechanism-based neuroprotective interventions, such as acamprosate and memantine, have attempted. Further prospective and well-designed studies of neuroprotective interventions against neurotoxic effects of alcohol are required.
Acetaldehyde ; Brain ; Drinking ; Drinking Behavior ; Female ; Glutamic Acid ; Humans ; Memantine ; Neuroimaging ; Oxidative Stress ; Taurine

BACKGROUND AND OBJECTIVES: Tinnitus is one of the most widespread disorders of the auditory system, affecting approximately 17% of the general population, with the frequency increasing to about 33% in the elderly. However, little is known about the underlying physiological mechanism that causes tinnitus and there is no definite treatment. Recently, several studies have showed that subjective tinnitus is mostly generated at the synapse between inner hair cells and their afferent nerves and in addition, some have showed that glutamate is likely to act as the neurotransmitter. The aim of this study has been to evaluate the effective use of caroverine hydrochloride and memantine hydrochloride for tinnitus treatment and to determine their appropriate indication of glutamate antagonist therapy. MATERIALS AND METHOD: From May 1998 through June 2000, 188 patients with subjective tinnitus were treated with caroverine hydrochloride (Spamon(R)). Of the patients, 153 were followed, and 20 of these patients who did not respond to caroverine hydrochloride were treated additionally with memantine hydrochloride (Akatinol(R)). Audiological evaluations were performed in all of the patients. Pre and post-treatment status was analyzed by handicap inventories. RESULTS: Subjective tinnitus was improved in 55 (35.9%) of 153 patients who were treated with caroverine hydrochloride and 11 (55.0%) of 20 patients with memantine hydrochloride. The response group had tendency of shorter duration history of tinnitus than the non-response group. There was no difference between the response group and the non-response group in age, sex, site, and tinnitus characteristics. CONCLUSION: We suggest that glutamate antagonists such as caroverine hydrochloride and memantine hydrochloride can be used as an alternative modality for treatment of subjective tinnitus.
Aged ; Equipment and Supplies ; Excitatory Amino Acid Antagonists ; Glutamic Acid* ; Hair ; Humans ; Memantine ; Neurotransmitter Agents ; Synapses ; Tinnitus*