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FP Essentials Nov 2023Dementia management requires individualized patient encounters that focus on education and realistic expectations. Numerous vitamins and supplements are promoted for...
Dementia management requires individualized patient encounters that focus on education and realistic expectations. Numerous vitamins and supplements are promoted for memory enhancement, but they lack evidence to support their use. Nonpharmacotherapy should be used through all stages of dementia. Common initial pharmacotherapy includes cholinesterase inhibitors and memantine, with use guided by dementia type, tolerability, patient goals, and disease stage. Assessment of benefit should incorporate caregiver input, functional improvements, behavioral symptoms, and tolerability. Management length is individualized. When a drug is discontinued, physicians should evaluate the patient for early worsening of cognitive or functional symptoms. Newer treatments, such as aducanumab, can reduce beta-amyloid plaques, but evidence for cognitive improvements is lacking; these treatments also are expensive and patient access is limited, resulting in barriers to widespread use. As dementia progresses, patients often develop behavioral and psychological symptoms, which are challenging for patients and caregivers. Nonpharmacotherapy is the first-line treatment for behavioral and psychological symptoms of dementia. Use of antipsychotics and benzodiazepines should be limited unless symptoms are placing the patient or others in imminent danger. Pharmacotherapy for these symptoms should be individualized, often requiring trials of various therapeutic options.
Topics: Humans; Dementia; Antipsychotic Agents; Memantine; Cholinesterase Inhibitors; Caregivers
PubMed: 37976171
DOI: No ID Found -
Archives of Medical Research Oct 2020
Topics: Amantadine; Betacoronavirus; COVID-19; Coronavirus Infections; Humans; Pandemics; Parkinsonian Disorders; Pneumonia, Viral; SARS-CoV-2
PubMed: 32723524
DOI: 10.1016/j.arcmed.2020.07.002 -
Journal of Neural Transmission (Vienna,... Sep 2022The trajectory of the use of dopamine replacement therapy (DRT) in Parkinson's disease (PD) is variable and doses may need to be increased, but also tapered. The plan... (Review)
Review
The trajectory of the use of dopamine replacement therapy (DRT) in Parkinson's disease (PD) is variable and doses may need to be increased, but also tapered. The plan for dose adjustment is usually done as per drug information recommendations from the licensing bodies, but there are no clear guidelines with regards to the best practice regarding the tapering off schedule given sudden dose reductions of drugs such as dopamine agonists may have serious adverse consequences. A systematic literature search was, therefore, performed to derive recommendations and the data show that there are no controlled studies or evidence-based recommendations how to taper or discontinue PD medication in a systematic manner. Most of the data were available on the dopamine agonist withdrawal syndrome (DAWS) and we found only two instructions on how to reduce pramipexole and rotigotine published by the EMA. We suggest that based on the available data, levodopa, dopamine agonists (DA), and amantadine should not be discontinued abruptly. Abrupt or sudden reduction of DA or amantadine in particular can lead to severe life-threatening withdrawal symptoms. Tapering off levodopa, COMT inhibitors, and MAO-B inhibitors may worsen motor and non-motor symptoms. Based on our clinical experience, we have proposed how to reduce PD medication and this work will form the basis of a future Delphi panel to define the recommendations in a consensus.
Topics: Amantadine; Dopamine; Dopamine Agonists; Humans; Levodopa; Parkinson Disease; Substance Withdrawal Syndrome
PubMed: 34324057
DOI: 10.1007/s00702-021-02389-x -
Archives of Medical Research Oct 2020
Topics: Amantadine; Betacoronavirus; COVID-19; Coronavirus Infections; Humans; Pandemics; Parkinsonian Disorders; Pneumonia, Viral; SARS-CoV-2
PubMed: 32660794
DOI: 10.1016/j.arcmed.2020.07.001 -
Psychopharmacology Bulletin Feb 2023Memenatine is USFDA approved for dementia of Alzheimer's disease. Apart from this indication, trend of its use in psychiatry is on the rise addressing a multitude of... (Review)
Review
BACKGROUND
Memenatine is USFDA approved for dementia of Alzheimer's disease. Apart from this indication, trend of its use in psychiatry is on the rise addressing a multitude of disorders.
STUDY QUESTION
Memantine remains one of only few psychotropic drugs with antiglutamate activity. This might impart it a therapeutic potential in treatment-resistant major psychiatric disorders characterized by neuroprogression. We reviewed memantine basic pharmacology and its diversifying clinical indications while examining the extant evidence.
METHODS
EMBASE, Ovid MEDLINE, PubMed, Scopus, Web of Science, and Cochrane Database of Systemic Reviews were searched for all relevant studies up to date of November, 2022.
RESULTS
Sound evidence supports use of memantine for major neuro-cognitive disorder due to Alzheimer's disease and severe vascular dementia, obsessive-compulsive disorder, treatment-resistant schizophrenia, and, ADHD. Modicum evidence supports use of memantine for PTSD, GAD and pathological gambling. Less compelling evidence is present for use in catatonia. No evidence supports use for core symptoms of autism spectrum disorder.
CONCLUSIONS
Memantine is an important addition to the psychopharmacological armamentarium. Level of evidence supporting the use of memantine in these off-label indications is highly variable, and hence, sound clinical judgment is necessary for its proper use and placement in real-life psychiatric practice and psychopharmacotherapy algorithms.
Topics: Humans; Memantine; Alzheimer Disease; Autism Spectrum Disorder; Psychiatry; Off-Label Use
PubMed: 36873917
DOI: No ID Found -
Scientific Reports Sep 2021Amantadine hydrochloride (HCl) is commonly prescribed for treating influenza A virus infection and Parkinson's disease. Recently, several studies have indicated that the...
Amantadine hydrochloride (HCl) is commonly prescribed for treating influenza A virus infection and Parkinson's disease. Recently, several studies have indicated that the use of amantadine HCl is associated with corneal edema; however, the cytotoxic effect of amantadine HCl has not been investigated. In the present study, the effects of amantadine HCl on cell growth, proliferation, and apoptosis in bovine cornea endothelial cells, and in vitro endothelial permeability were examined. Results showed that lower doses of amantadine HCl do not affect cell growth (≤ 20 μΜ), whereas higher doses of amantadine HCl inhibits cell growth (≥ 50 μΜ), induces apoptosis (2000 μΜ), increases sub-G1 phase growth arrest (2000 μΜ), causes DNA damage (≥ 1000 μΜ), and induces endothelial hyperpermeability (≥ 1000 μΜ) in bovine cornea endothelial cells; additionally, we also found that amantadine HCl attenuates the proliferation (≥ 200 μΜ) and arrests cell cycle at G1 phase (≥ 200 μΜ) in bovine cornea endothelial cells. In the present study, we measured the cytotoxic doses of amantadine HCl on cornea endothelial cells, which might be applied in evaluating the association of corneal edema.
Topics: Amantadine; Animals; Antiviral Agents; Apoptosis; Cattle; Cell Cycle; Cell Proliferation; Cells, Cultured; Cornea; Endothelial Cells; Endothelium, Corneal
PubMed: 34531501
DOI: 10.1038/s41598-021-98005-9 -
European Journal of Neurology Apr 2022Levodopa-induced dyskinesia (LID) is a common motor complication in patients with Parkinson's disease (PD). Although amantadine is indicated for LID treatment, it is...
BACKGROUND AND PURPOSE
Levodopa-induced dyskinesia (LID) is a common motor complication in patients with Parkinson's disease (PD). Although amantadine is indicated for LID treatment, it is uncertain whether early treatment with amantadine reduces the risk of LID in patients with PD. We aimed to evaluate the association between amantadine treatment and LID onset in patients with early-stage PD.
METHODS
This was a hospital-based retrospective cohort study that used electronic medical records from January 1, 2009 to October 31, 2016. The effect of amantadine on LID onset was compared with those of anticholinergics and monoamine oxidase type B inhibitors in patients with PD. Propensity-score weighting and landmark analysis were used to reduce potential confounding. The time to LID onset was analyzed using Cox models. Sensitivity analyses were performed to determine the robustness of the results.
RESULTS
The analyses included 807, 661, and 518 patients at 6-, 12-, and 18-month landmark points, respectively. Amantadine use was associated with delayed LID onset in the 6- and 12-month landmark analyses, with adjusted hazard ratios of 0.65 (95% confidence interval [CI] = 0.49-0.86) and 0.64 (95% CI = 0.47-0.88), respectively. Sensitivity analysis findings were comparable to those of the main analysis.
CONCLUSIONS
Early treatment with amantadine may delay LID onset more than treatment with other symptomatic agents. Further studies are needed to elucidate the mechanism of amantadine in LID onset delay and to validate our findings.
Topics: Amantadine; Antiparkinson Agents; Dyskinesia, Drug-Induced; Humans; Levodopa; Parkinson Disease; Retrospective Studies
PubMed: 34962701
DOI: 10.1111/ene.15234 -
Neuropharmacology Feb 2024The great potential for NMDA receptor modulators as druggable targets in neurodegenerative disorders has been met with limited success. Considered one of the rare... (Review)
Review
The great potential for NMDA receptor modulators as druggable targets in neurodegenerative disorders has been met with limited success. Considered one of the rare exceptions, memantine has consistently demonstrated restorative and prophylactic properties in many AD models. In clinical trials memantine slows the decline in cognitive performance associated with AD. Here, we provide an overview of the basic properties including pharmacological targets, toxicology and cellular effects of memantine. Evidence demonstrating reductions in molecular, physiological and behavioural indices of AD-like impairments associated with memantine treatment are also discussed. This represents both an extension and homage to Dr. Chris Parson's considerable contributions to our fundamental understanding of a success story in the AD treatment landscape.
Topics: Humans; Memantine; Alzheimer Disease; Receptors, N-Methyl-D-Aspartate; Cognition
PubMed: 37832633
DOI: 10.1016/j.neuropharm.2023.109737 -
Physical Medicine and Rehabilitation... Feb 2024Pharmacologic treatment of disorders of consciousness remains a critical but challenging task for clinicians. Amantadine has been shown to promote the rate of neurologic... (Review)
Review
Pharmacologic treatment of disorders of consciousness remains a critical but challenging task for clinicians. Amantadine has been shown to promote the rate of neurologic recovery for patients with traumatic disorders of consciousness when administered between 4 and 16 weeks, as demonstrated by a well-designed randomized control trial. While there are no large, randomized controlled trials to support the use of other dopaminergic medicines (bromocriptine, levodopa, apomorphine), there is a large body of literature implicating their role in improving alertness and responsiveness in disorders of consciousness. Zolpidem can increase the level of consciousness in a small subset of patients. Zolpidem and intrathecal baclofen likely increase the level of consciousness via the mesocircuit pathway. Psychostimulant medications can be initiated in patients, even without strong evidence to support their use, as long as basic principles of brain injury medicine are followed, and there are systems in place to evaluate therapeutic response.
Topics: Humans; Consciousness; Zolpidem; Consciousness Disorders; Brain Injuries; Amantadine; Randomized Controlled Trials as Topic
PubMed: 37993186
DOI: 10.1016/j.pmr.2023.06.023 -
Clinical NeuropharmacologyAcute traumatic brain injury is one of the most common causes of death and disability. Reduction in the level of consciousness is a significant complication that can...
OBJECTIVES
Acute traumatic brain injury is one of the most common causes of death and disability. Reduction in the level of consciousness is a significant complication that can impact morbidity. Glasgow Coma Scale (GCS) is the most widely used method of assessing the level of consciousness. Neurostimulants such as amantadine and modafinil are common pharmacologic agents that increase GCS in patients with brain trauma. This study aimed to compare the effectiveness of these 2 drugs.
METHODS
This systematic review obtained articles from Google Scholar, PubMed, Scopus, Embase, and MEDLINE databases. Extensive searches were conducted separately by 4 individuals in 3 stages. Ultimately, 16 clinical trials, cohort studies, case reports, and case series articles were obtained after reading the title, abstract, and full text and considering the exclusion criteria. The data of the final article were entered into the analysis table. This study was registered with PROSPERO (registration number CRD42022334409) and conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.
RESULTS
Amantadine seems to be associated with a higher overall response rate. In contrast, modafinil is associated with the most remarkable change in GCS score during treatment. However, the number of clinical trials with high quality and sample size has not been satisfactory to compare the effectiveness of these 2 drugs and their potential side effects.
CONCLUSIONS
The authors recommend additional double-blind clinical trials are needed to be conducted with a larger sample size, comparing amantadine with modafinil to delineate the efficacy and adverse effects, both short and long term.
Topics: Humans; Modafinil; Consciousness; Brain Injuries, Traumatic; Amantadine; Brain Injuries; Randomized Controlled Trials as Topic
PubMed: 37962310
DOI: 10.1097/WNF.0000000000000577