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Symmetrel

Generic Symmetrel is an antiviral medication. It blocks the actions of viruses in your body. Generic Symmetrel is used to treat and prevent influenza A (viral infection). Generic Symmetrel is also used to treat Parkinson's disease and "Parkinson-like" symptoms such as stiffness and shaking that may be caused by the use of certain drugs.

Other names for this medication:

Similar Products:
Famvir, Rebetol, Sustiva, Combivir, Epivir, Retrovir

 

Also known as:  Amantadine.

Description

Generic Symmetrel is an antiviral medication. It blocks the actions of viruses in your body.

Generic name of Generic Symmetrel is Amantadine.

Symmetrel is also known as Amantadine.

Brand name of Generic Symmetrel is Symmetrel.

Dosage

Take this medicine with a full glass of water. If you are taking Generic Symmetrel to treat influenza A, start taking the medication within 24-48 hours after flu symptoms begin.

Do not stop taking it suddenly.

Overdose

If you overdose Generic Symmetrel and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Symmetrel are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Be careful with Generic Symmetrel while you are pregnant or have nurseling. Generic Symmetrel can pass in breast milk and harm your baby.

Do not use Generic Symmetrel if you are allergic to Generic Symmetrel components.

Do not use FluMist nasal influenza "live vaccine" while you are being treated with Generic Symmetrel and for at least 48 hours after you stop taking Generic Symmetrel. The nasal vaccine may not be as effective if you receive it while you are taking Generic Symmetrel.

Be careful with Generic Symmetrel if you have epilepsy or other seizure disorder, congestive heart failure, kidney or liver disease, low blood pressure, eczema, glaucoma, or a history of mental illness, suicide attempt, or drug/alcohol addiction.

Be careful with Generic Symmetrel if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Generic Symmetrel if you take atropine (Atreza, Sal-Tropine, and others); dicyclomine (Bentyl); glycopyrrolate (Robinul); hyoscyamine (Anaspaz, Levbid, Levsin, Nulev, and others); mepenzolate (Cantil); methscopolamine (Pamine); propantheline (Pro-Banthine); scopolamine (Maldemar, Scopace, Transderm-Scop); quinine (Qualaquin); quinidine (Cardioquin, Quinaglute); diuretic (water pill) such as triamterene (Dyrenium), hydrochlorothiazide (HCTZ, Dyazide, HydroDiuril, Hyzaar, Lopressor, Vasoretic, Zestoretic); phenothiazines such as prochlorperazine (Compazine), thioridazine (Mellaril), and others.

Avoid alcohol.

Do not stop taking it suddenly.

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Antiviral agents are less numerous and often more toxic than antibacterial agents. Acyclovir is commonly used for suppression and treatment of recurrent genital herpes simplex virus and may be indicated for pregnant women with disseminated herpes. Zidovudine is indicated for pregnant women with human immunodeficiency virus infection who have low CD4 lymphocyte counts. Ganciclovir, vidarabine, ribavirin, amantadine, didanosine, and foscarnet are rarely indicated in gynecology and are not recommended for use in pregnancy.

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Cholinesterase inhibitors and memantine are widely used for the treatment of Alzheimer disease (AD) and other non-AD dementia worldwide. Since 2000, large scale prospective random control studies using meta-analysis have provided clinical evidence for the use of these drugs in AD and non-AD dementia. Here, we review these reports, including those on other drugs and newly developed drugs, which provide detailed clinical information for the daily management of dementia.

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The dependence of the surface potential difference (delta U), transversal elasticity module (E1) and membrane conductivity (G0) on the concentrations of the antiviral drugs, rimantadine and amantadine was studied in the planar bilayer lipid membrane system. The method used was based on independent measurements of the second and third harmonics of the membrane capacitance current. The binding constants of bilayer lipid membranes obtained from the drug adsorption isotherms were 2.1 X 10(5) M-1 and 1.3 X 10(4) M-1 for rimantadine and amantadine, respectively. The changes in G0 took place only after drug adsorption saturation had been achieved. The influence of rimantadine and amantadine on the interaction of bilayer lipid membranes with matrix protein from influenza virus was also investigated. The presence of 70 micrograms/ml rimantadine in the bathing solution resulted in an increase in the concentration of M-protein at which the adsorption and conductance changes were observed. The effects of amantadine were similar to those of rimantadine but required a higher critical concentration of amantadine. The results obtained suggest that the antiviral properties of rimantadine and amantadine may be related to the interaction of these drugs with the cell membrane, which can affect virus penetration into the cell as well as maturation of the viral particle at the cell membrane.

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This economic evaluation indicates that institutionalization is the largest cost component in AD management and that the use of memantine, combined with a ChEI, to treat AD is a cost-effective alternative, compared with the use of a ChEI alone.

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One of the biggest challenges in the effort to treat and contain influenza A virus infections is the emergence of resistance during treatment. It is well documented that resistance to amantadine arises rapidly during the course of treatment due to mutations in the gene coding for the M2 protein. To address this problem, it is critical to develop experimental systems that can accurately model the selection of resistance under drug pressure as seen in humans. We used the hollow-fiber infection model (HFIM) system to examine the effect of amantadine on the replication of influenza virus, A/Albany/1/98 (H3N2), grown in MDCK cells. At 24 and 48 h postinfection, virus replication was inhibited in a dose-dependent fashion. At 72 and 96 h postinfection, virus replication was no longer inhibited, suggesting the emergence of amantadine-resistant virus. Sequencing of the M2 gene revealed that mutations appeared at between 48 and 72 h of drug treatment and that the mutations were identical to those identified in the clinic for amantadine-resistant viruses (e.g., V27A, A30T, and S31N). Interestingly, we found that the type of mutation was strongly affected by the dose of the drug. The data suggest that the HFIM is a good model for influenza virus infection and resistance generation in humans. The HFIM has the advantage of being a highly controlled system where multiplicity parameters can be directly and accurately controlled and measured.

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Twenty-four subjects with Huntington disease took amantadine hydrochloride, 100 mg 3 times daily for 2 weeks, and placebo for 2 weeks.

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The cellular localization of organic cation transporter (OCT) 1 and OCT2 in isolated brain microvessel endothelial cells from humans, rats, and mice and in cultured adult rat brain endothelial cells was examined by confocal microscopy and in isolated luminal and abluminal membrane fractions by Western blot analysis. Cellular uptake of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was measured with or without OCT1/OCT2 silencing. The interaction between MPTP and amantadine was studied by in vitro kinetic analysis and in vivo brain microdialysis. MPTP-induced dopaminergic toxicity was examined by measuring dopamine levels in the brain striatum and by positron emission tomography scanning. The results showed that both OCT1 and OCT2 were mainly expressed on the luminal side of brain microvessel endothelial cells and adult rat brain endothelial cells. Cellular uptake of MPTP was significantly (p < 0.05) decreased by about 53%, 60%, or 91% following silencing of OCT1, OCT2, or both, respectively. Amantadine competitively inhibited MPTP uptake in vitro and significantly (p < 0.05) reduced the area under the time-concentration curve for MPTP and MPP(+) in the brain extracellular fluid in rats and mice by 65-70% and 35-85%, respectively. MPTP-induced dopaminergic toxicity in mice was ameliorated by amantadine without stimulating dopamine turnover. In conclusion, OCT1 and OCT2 are important for MPTP transfer across the blood-brain barrier and amantadine reduces the blood-brain barrier transfer of MPTP and MPTP-induced dopaminergic toxicity in rodents.

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Novel antipsychotics (clozapine, risperidone, olanzapine, quetiapine) are effective in treating psychotic symptoms, also in neurological disease. Hyperprolactinemia is a side effect related to antipsychotics that can cause galactorrhea, gynecomastia, amenorrhea, anovulation, impaired spermatogenesis, decreased libido and sexual arousal, impotence, and anorgasmia, consequent to removal of tonic dopaminergic inhibition of prolactin secretion via hypothalamic dopaminergic receptor blockade in the tuberoinfundibolar tract. Hyperprolactinemia occurs more frequently during treatment with risperidone and olanzapine compared with clozapine and quetiapine. The therapeutic algorithm to antipsychotic-relatedhyperprolactinemia is the following: reduction in antipsychotic dose, addition of cabergoline, bromocriptine, amantadine, and/or switch to another antipsychotic. We propose switching to quetiapine in symptomatic hyperprolactinemia related to antipsychotics and describe five cases.

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Immunocompromised patients are at increased risk of complications of influenza virus infection. We report on two critically ill patients on immunosuppressive medication with influenza pneumonia. In both patients, oseltamivir monotherapy did not result in clearance of the virus after 18 and five days, respectively. After adding zanamivir and amantadine to the treatment, PCRs on pharyngeal and/or plasma specimens turned negative in both patients after four and three days, respectively. We suggest, that in critically ill patients with influenza A H1N1 infection, treatment efficacy should be monitored closely and treatment with a combination of antiviral drugs should be considered.

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Antiviral susceptibility surveillance in the Netherlands was intensified after the first reports about the emergence of influenza A(H1N1) oseltamivir resistant viruses in Norway in January, 2008.

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Patients with chronic hepatitis C infection should be assessed by liver biopsy prior to consideration of anti-viral therapy. Patients with histologically mild disease should be observed at regular intervals and assessed with a repeat liver biopsy after an interval of 3-4 years. Those with severe disease should receive early treatment with interferon-alpha and ribavirin. The duration of therapy is determined by the genotype of the infecting virus-viral genotypes 2 and 3 require only 6 months of treatment but other genotypes should be treated for 12 months. Approximately 35-40% of treated patients will respond to therapy with a permanent cessation of viral replication and improvement in liver histology. New therapies including polyethylene glycol, PEGylated, interferons and combination regimes involving amantadine are currently under evaluation and it is hoped that improved regimes will be developed in the near future.

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The prevalence of ICBs in PD patients is approximately 3-4% for DDS, 0.34-4.2% for punding, and 6-14% for ICDs, with higher prevalence in Western populations than in Asian. Those who take high dose of levodopa are more prone to have DDS, whereas, ICDs are markedly associated with dopamine agonists. Different subtypes of ICBs share many risk factors such as male gender, higher levodopa equivalent daily dose, younger age at PD onset, history of alcoholism, impulsive, or novelty-seeking personality. The Questionnaire for Impulsive-Compulsive Disorder in Parkinson's Disease-Rating Scale seems to be a rather efficacious instrument to obtain relevant information from patients and caregivers. Treatment of ICBs is still a great challenge for clinicians. Readjustment of DRT remains the primary method. Atypical antipsychotics, antidepressants, amantadine, and psychosocial interventions are also prescribed in controlling episodes of psychosis caused by compulsive DRT, but attention should be drawn to balance ICBs symptoms and motor disorders. Moreover, deep brain stimulation of the subthalamic nucleus might be a potential method in controlling ICBs.

symmetrel drug summary

At 30-microM concentrations, the genistein, resveratrol, and memantine inhibitors were able to reverse significantly the loss of cell viability, the activation of caspase-3/7 and caspase-9, and the production of ROS/RNS in ARPE-19 cell cultures. Memantine was the most potent and genistein was the least effective inhibitor in blocking the B(e)P-induced effects. Calpain, BITC, simvastatin, and epicatechin did not reverse the loss of cell viability in B(e)P-treated ARPE-19 cells. As a matter of fact, at the concentrations studied (15, 30, 45 microM), the BITC plus B(e)P-treated cultures showed significantly lower cell viability than the B(e)P-treated culture alone, suggesting BITC-related toxicity.

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Outbreak investigation with predetermined and concurrently determined risk information.

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While clinicians are familiar with psychosis as a complication in the long-term treatment with amantadine, rapid psychiatric complications are of much less concern. In the case presented, severe decompensation in mental status occurred within 48 h of initiation of standard doses of amantadine hydrochloride. Clinicians should be alert not only for delayed complications but also for early-onset mental decompensation in elderly patients with influenza A treated with amantadine.

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A nationally representative survey of experts in geriatric clinical pharmacy.

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An experimental medicine model to assess acute pro-cognitive drug effects in CPD subjects is feasible but not without challenges. A single MEM 20 mg dose had a negative impact on neurocognition among HS. In CPD patients, age, MEM effects on PPI, and rs1337697 predicted sensitivity to the neurocognitive effects of MEM. Any potential clinical utility of these predictive markers for pro-cognitive effects of MEM in subgroups of CPD patients cannot be inferred without a validating clinical trial.

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In this randomised, double-blind, placebo-controlled pilot study, 36 patients with moderate AD received 52 weeks of memantine (20 mg/day) or placebo. Patients were re-evaluated after 26 and 52 weeks to measure the change from baseline in several outcome measures including global and regional glucose metabolism, total brain and hippocampal volumes, as well as chemical shift imaging-derived global and regional N-acetylaspartate and myoinositol concentrations.

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There is solid evidence that retreatment of non-responders with standard regimens of interferon monotherapy is of no clinical value. On the other hand, combination therapy with interferon and ribavirin now produces sustained response rates in non-responders similar to those of interferon monotherapy in untreated patients. Consequently, retreatment of non-responders with the combination of interferon-ribavirin appears to be a valid treatment option. The efficacy of retreatment with the interferon-ribavirin combination can probably be increased by modifying the first weeks of interferon therapy from standard (3 MU tiw) to induction (10 MU daily), and by extending the treatment period to 12 months. In the next few years, the additive value of amantadine to interferon or to interferon-ribavirin combination in inducing sustained viral clearance should be explored. For the many patients who still do not respond with viral clearance despite these new approaches, the goal of therapy might be shifted towards persistent ALT normalization in order to reduce the progression of liver disease. Drugs that can normalize serum ALT such as interferon, ursodeoxycholic acid, ribavirin and glycyrrhizin should be evaluated for this objective.

symmetrel reviews

Naloxone increased ratings and produced physical changes consistent with opioid withdrawal. Memantine attenuated the severity of opioid withdrawal as assessed with the Clinical Institute for Narcotic Withdrawal Scale scale. Withdrawal was significantly reduced when naloxone was administered at 6 and 52 h after memantine, but not when administered 126 h (5 days) after memantine. Medication effects, assessed 5 h after memantine administration and before naloxone administration, included significant increases in ratings of "strong" and "good" drug effect, and "I feel sedated", "mellow", and "high".

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Behavioural disturbances are a common and distressing aspect of Alzheimer's disease (AD). This pooled analysis evaluated the specific benefits of memantine on behavioural disturbances in patients with moderate to severe AD.

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Glutamate is stored in platelet dense granules and large amounts (>400 μM) are released during thrombus formation. N-methyl-d-aspartate glutamate receptors (NMDARs) have been shown in platelets but their roles are unclear.

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Imatinib is a substrate for hOCT1 (SLC22A1) and inhibitors of this influx transporter, such as amantadine and prazosin, have previously been shown to decrease cellular imatinib uptake. However, here we report that in longer term experiments, both drugs paradoxically increase the cytotoxicity of all three currently licensed tyrosine kinase inhibitors (TKIs), imatinib, nilotinib and dasatinib. This effect is due to release of intracellular calcium from the endoplasmic reticulum (ER), with changes in mitochondrial calcium and alterations in mitochondrial membrane permeability, resulting in caspase-mediated apoptosis. The effect is confined to BCR-ABL-positive cells, and is greater in primary cells than in cell lines. Furthermore, in primary cells at original diagnosis, the effect is only seen in samples from patients destined to become complete cytogenetic responders to imatinib. These results indicate that calcium release from the ER, here induced by amantadine or prazosin, may prime BCR-ABL-positive cells to TKI-induced apoptosis. Amantadine/prazosin primed TKI cytotoxicity in vitro may be a useful test for the level of ER-releasable calcium, and may be of prognostic value.

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The present study aimed to evaluate the discriminative-stimulus effects of the NMDA receptor channel blockers (+)MK-801, dextromethorphan, and memantine in rats trained to discriminate nicotine from its vehicle.

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To evaluate the antiviral activity and the safety of amantadine (200 mg daily for 6 months) in elderly patients with chronic hepatitis C.

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Sildenafil is beneficial in reversing female sexual dysfunction induced by SSRIs. This paper also discusses sildenafil's action in the background of nitric oxide and cyclic guaninosine monophosphate in penile/clitoral erection.

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After blockade of cutaneous trunci muscle reflex with subcutaneous injections, we evaluated the cutaneous analgesic effect of memantine, lidocaine, and dizocilpine (MK-801) in rats. The dose-dependent response of memantine on cutaneous analgesia was compared with lidocaine and MK-801 in rats. The duration of action for each drug was evaluated and compared on an equipotent basis (20% effective dose [ED(20)], ED(50), and ED(80)). Lidocaine, a frequently used local anesthetic, was used as control.

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symmetrel drug class 2017-01-30

Fatigue is a common symptom in patients with multiple sclerosis. Rapid exhaustion and reduced exercise tolerance leads to difficulties in maintaining a normal daily life for many patients. Regular resting and short breaks can help to compensate this to a certain degree. The pathophysiology of fatigue is currently unknown. Damage of specific neuroanatomic regions or a more generalized effect of inflammatory mediators in the central nervous system could be the causes of fatigue. Some drugs (e.g. amantadine) have proven effective in therapy of fatigue. Recent therapeutic approaches have begun using aminopyridines (4-aminopyridine, 3, buy symmetrel 4-diaminopyridine). These two substances are thought to improve nerve conduction, but there might be a central stimulatory effect as well. Overdosage leads to an elevated risk of epileptic seizures and confusion.

symmetrel drug summary 2017-08-29

We consider the sample pretreatment without deproteination, derivatization and centrifugation steps and the specificity of the tandem mass spectrometry as the most important points buy symmetrel of our amantadine analysis method.

symmetrel capsules 2017-08-15

Methanol poisoning is an uncommon but potent central nervous system toxin. The diagnosis and the management of its sequelae remain a challenge to clinicians. A case is hereby presented in which computed tomography of the brain played buy symmetrel an important role in making the diagnosis due to poor patient's history and unavailability of methanol assay. Parkinsonism and visual sequelae are well-recognised complications in the survivors. This patient developed parkinsonism in the form of mainly severe tremors and mild rigidity. He benefited from treatment on amantadine.

symmetrel dosage forms 2017-12-18

Memantine (MN), a NMDA blocker is well known for its protective effect against various neurodegenerative diseases. However, its role in improving motor function and regulation of neurotrophic factors in Huntington's disease (HD) has not been studied yet. In the present study, we have investigated the effect of MN against 3-nitropropionic acid (3NP), induced motor impairment, and alterations in the expression of brain-derived neurotrophic factor (BDNF) and glial cell- buy symmetrel derived neurotrophic factor (GDNF) in mice brain. Further, its role in mitochondrial function was assessed by measuring succinate dehydrogenase (SDH) activity. Glial fibrillary acidic protein (GFAP) and neuronal nuclei (NeuN) immunoreactivity were studied to evaluate the role of MN on glial and neuronal function. Its effect on apoptosis was adjudged by studying the expression of apoptotic markers. MN restored motor functions with an associated up-regulation in neurotrophin expression. MN also enhanced brain SDH activity and decreased glutamate content. MN ameliorated striatal neuronal loss, reduced GFAP immunoreactivity, and exhibited protective effect against neuronal apoptosis. Data from the current study demonstrated that MN exerted neuroprotective effect against 3NP induced neuropathology. Restoration of motor function by MN might be through regulation of neurotrophin expression. MN can therefore be a useful therapeutic choice in the symptomatic management of HD.

symmetrel dosage 2016-07-19

To investigate the changes in buy symmetrel cerebral glucose metabolism in patients with posttraumatic cognitive impairment after memantine therapy.

symmetrel medication 2015-01-14

Our objective is to describe the results of a phase II/III, 12-months, double-blinded, single-centre, randomized, parallel (1:1), clinical trial performed to evaluate the efficacy and safety of memantine in ALS. Patients with probable or definite ALS of less than 36 months disease duration and progression over a one- buy symmetrel month lead-in period were randomly assigned to placebo or memantine at 20 mg/day. The primary endpoint was 12-months ALSFRS decline. Forced vital capacity, manual muscle testing, visual analogue scale, quality of life, motor unit number estimation and neurophysiological index were the secondary endpoints. The number of patients included was based on the assumption of a 50% change in the ALSFRS decline. Safety and adverse events were evaluated. Sixty-three patients were included in the trial. Memantine did not show more adverse events or laboratory changes than placebo. Primary and secondary outcomes were not different between groups by intention-to-treat and per-protocol analysis. The most sensitive measurements were neurophysiological, which declined linearly over time. In conclusion, the results of this study show that memantine is well tolerated and safe in ALS patients. We did not observe any evidence of efficacy for memantine but we cannot exclude a positive outcome on survival.

symmetrel drug interactions 2015-07-26

Randomized, observer-blinded comparison buy symmetrel of regimes.

symmetrel medication cost 2017-12-17

Influenza poses special hazards inside healthcare facilities and can cause explosive outbreaks of illness. Healthcare workers are at risk of acquiring influenza and thus serve as an important reservoir for patients under their care. Annual influenza immunisation of high-risk persons and their contacts, including healthcare workers, is the primary means of preventing nosocomial influenza. Despite influenza vaccine effectiveness, it is substantially underused by healthcare providers. Influenza can be diagnosed by culturing the virus from respiratory secretions and by rapid antigen detection kits; recognition of a nosocomial outbreak is important in order to employ infection- buy symmetrel control efforts. Optimal control of influenza in the acute-care setting should focus upon reducing potential influenza reservoirs in the hospital, including: isolating patients with suspected or documented influenza, sending home healthcare providers or staff who exhibit typical symptoms of influenza, and discouraging persons with febrile respiratory illness from visiting the hospital during a known influenza outbreak in the community. (Note: influenza and other respiratory viruses can cause non-febrile illness but are still transmissible.) The antiviral M2 protein inhibitors (amantadine, rimantadine) and neuraminidase inhibitors (zanamivir, oseltamivir) have proven efficacy in treating and preventing influenza illness; however, their role in the prevention and control of influenza in the acute hospital setting remains to be more fully studied.

symmetrel brand name 2017-03-21

The efficacy and tolerability of memantine (1-amino-3,5-dimethyl-adamantane hydrochloride, Akatinol Memantine; CAS 41100-52-1) was investigated in a double-blind, randomized clinical study versus placebo in 66 patients aged between 65 and 80 years predominantly suffering from mild to moderate vascular dementia. The target variables assessed were the baseline differences buy symmetrel of the Sandoz Clinical Assessment Geriatric scale (SCAG) and Syndrom-Kurz-Test (SKT) total scores and the total time required in the subtests of Activity of Daily Living tests (ADL). Additional parameters assessed were the physician's global impression, the Mini Mental State Evaluation (MMSE), the Tapping and Trace tests for fine motor rating and the quality in performing the ADL tests. Adverse drug effects were recorded by DOTES/TWIS. 59 of the 66 patients included in the study terminated the trial (29 in the placebo and 30 in the memantine group). For the baseline differences of the SCAG total score a statistically significant improvement was observed already after 14 days of memantine treatment as compared to placebo. After 42 days this difference was still more pronounced and highly significant. Significant improvements after 14 and 42 days of memantine treatment could also be demonstrated for the SCAG subscales cognitive disturbances, lack of drive, emotional disturbances, social behaviour and somatic disturbances. Additionally, the efficacy of the drug could be confirmed by the SKT and ADL tests. Particularly striking in the ADL tests was the considerable improvement achieved in the quality of performing the tasks under memantine treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

symmetrel generic 2017-08-01

Levodopa is extremely effective in controlling many of the symptoms of Parkinson's disease (PD) and will be required by most patients during the course of the disease. However,levodopa therapy is associated with certain drawbacks, including the inability to control some PD symptoms, such as autonomic disturbances and neuropsychiatric symptoms, and the occurrence of motor complications with chronic treatment. Wearing off refers to a waning of response to levodopa prior to the next dose, resulting in fluctuations in motor function. AsPD progresses, the therapeutic window of response to levodopa narrows, making it difficult to find a dose that controls symptoms without resulting in dyskinesia. Motor complications are believed to be due to the progressive loss of dopaminergic neurons that results in a decreased ability to buffer fluctuations in dopamine levels in the brain,coupled with the short half-life of levodopa. Motor complications occur in over 90% of patients who have been treated with levodopa for more than 10 years and are associated with reduced function, reduced quality of life, and high treatment costs. Strategies to manage motor complications include delaying the initiation of levodopa therapy when possible, altering levodopa doses or frequency of administration, and adding adjunct therapies. Catechol-O-methyltransferase (COMT)inhibitors extend the half-life of levodopa and result in significant reductions in off times in patients with motor fluctuations. Dopamine agonists, monoamine oxidase-B (MAO buy symmetrel -B)inhibitors, and amantadine are other candidates for adjunct therapies. Dyskinesia is usually managed through changes in levodopa dosing or administration; changing the doses of adjunct therapies also may be helpful.

symmetrel 200 mg 2016-10-08

There were no statistically significant differences in the rates of change in TBV, ventricular volume, or left hippocampal volume between the study periods; however, the memantine treatment period was associated with a significantly slower right hippocampal atrophy (-5.5% ± 12.0% vs -10.8% ± 7.2%; P = .038). Memantine treatment was also associated with superior performances on the Boston Naming Test (P = .034) and the Trail Making Test, Part B (P = .001), but also with a higher number of errors (i.e., repetitions and intrusions) on the California Verbal Learning Test. Memantine was found to be safe and buy symmetrel well tolerated.

symmetrel overdose 2016-02-07

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 buy symmetrel 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).

symmetrel generic name 2015-11-15

The paper describes the effect of amantadine (AMA) supplementation on imipramine (IMI) therapy in patients (with treatment-resistant unipolar depression) who fulfilled DSM IV criteria for major depression. Twelve patients were enrolled to the study on the basis of history of their illness and therapy. Following 2 weeks of washout period, the patients were treated with IMI twice daily (100-150 mg/day) for 6 weeks, and then AMA was introduced (twice buy symmetrel daily, 100-150 mg/day) and administered jointly with IMI for further 6 weeks. Thereafter, AMA was withdrawn, and the patients were treated with IMI alone for 2 weeks. Hamilton Depression Rating Scale (HDRS) and Beck Depression Inventory (BDI) were used to assess efficacy of antidepressant therapy. IMI changed neither HDRS nor BDI score after 3 or 6 weeks of treatment when compared with washout (before treatment). AMA supplementation significantly reduced both HDRS and BDI scores after 3- or 6-week supplementation. AMA augmentation of IMI treatment was beneficial and lasted even after AMA withdrawal. Moreover, pharmacokinetic data indicate that AMA did not influence significantly the plasma concentration of the IMI and its metabolite, desipramine, in the patients during joint treatment with AMA and IMI, what suggests the lack of pharmacokinetic interaction. These results suggest that joint therapy with IMI and AMA may be successful in the treatment-resistant unipolar depression.

symmetrel en alcohol 2017-03-04

We performed a randomized, double-masked, placebo-controlled study investigating the effects of memantine and gabapentin on congenital nystagmus over a period of 56 days. The primary outcome measure was logarithmic minimum angle of resolution (logMAR) visual acuity; the secondary outcome measures were nystagmus intensity and foveation, Avapro 20 Mg subjective questionnaires about visual function (VF-14) and social function. Analyses were by intention to treat.

symmetrel drug classification 2015-11-25

In a pilot study, 29 outpatients with bipolar depression on a stable lamotrigine dose regimen received placebo or memantine pills daily (titrated up by 5 mg week⁻¹ to 20 mg) in a randomized, double-blind, parallel group, 8 week study. Patients were evaluated weekly using the 17-item Hamilton Depression Rating Score (HDRS) and all data were analyzed simultaneously. Linear, exponential, maximal effect, Gompertz and inverse Bateman functions were evaluated using a Bayesian approach population pharmacodynamic model framework. In these Medicine Zovirax models, differences in parameters were examined across the memantine and placebo augmentation groups.

symmetrel user reviews 2015-03-07

To assess management strategies for paediatric patients suffering from Zithromax 500mg Online concussions.

symmetrel drug 2016-09-19

Neuroleptic malignant syndrome (NMS) is a rare life-threatening disorder resulting from treatment with neuroleptic agents and other drugs that act as dopamine antagonists. NMS most often occurs shortly after the initiation, dose increase or withdrawal of the offending agent, but can rarely occur after long-term treatment at stable doses. Immediate discontinuation of the causative agent (or re-administration if the cause is the withdrawal of neuroleptic Diamox 125 Mg therapy) along with supportive therapy to maintain cardiorespiratory stability and to reduce fever are the cornerstone of the management of NMS. Additional 'specific' treatments include dantrolene, bromocriptine and amantadine, but their role in the management of NMS is controversial.

symmetrel buy 2016-12-17

In continuing the search for fluorescent reagents for analytical derivatization in chromatography, we found a simple chemical, (2-naphthoxy)acetyl chloride, with potential fluorophore/chromophore characteristics for the highly sensitive detection of analytes with an amino function. The reagent has an auxochrome (a substituted alkoxy moiety) attached to the fluorophoric/chromophoric naphthalene system, resulting in favorable spectrophotometric properties. The reagent can be easily prepared from (2-naphthoxy)acetic acid Diflucan 50mg Dosage and has been used in organic synthesis; it is initially introduced as a fluorescent reagent to derivatise amantadine and memantine (amino pharmaceuticals) as model analytes. The resulting naphthoxy derivatives of the drugs can be analyzed at sub-microM levels by HPLC with fluorimetric detection (excitation wavelength 227 nm, emission wavelength 348 nm). Application of the reagent to the fluorimetric derivatization of important biological amines for sensitive detection can be expected.

symmetrel cost 2015-10-01

Phenotypic and molecular studies were conducted to characterize multiple influenza A isolates recovered from an immunocompromised patient who died of viral and fungal pneumonitis. The recovery of amantadine- Requip And Alcohol resistant isolates was correlated with the detection of 2 drug-resistant M2 variants (codons 27 and 31) in combination with a wild-type virus. The mutant viruses persisted within the viral population in variable proportions >1 month after cessation of antiviral therapy. These results confirm animal studies reported elsewhere regarding the genetic stability of influenza M2 mutants and their potential for transmission in humans.

symmetrel 100mg capsules 2015-08-19

A chemically synthesized peptide consisting of the C-terminus of the M protein of the Dengue virus type 1 strain Singapore S275/90 (DVM-C) produced ion channel activity in artificial lipid bilayers. The channels had a variable conductance and were more permeable to sodium and potassium ions than to chloride ions and more permeable to chloride ions than to calcium ions. Hexamethylene amiloride (100 microM) and amantadine (10 microM), blocked channels formed by DVM-C. Ion channels may play an important role in the life cycle of many viruses and Plavix Tablet Uses drugs that block these channels may prove to be useful antiviral agents.

symmetrel pill 2015-09-07

Three of 687 (0.4%) A(H1N1) viruses from the 2007-2008 season and 745 of 745 (100%) viruses from the 2008-2009 season carried the NA-H274Y substitution and demonstrated a >300-fold reduction in oseltamivir susceptibility. All oseltamivir-resistant viruses from the 2008-2009 season possessed Asacol Generic 2014 an A193T substitution in the receptor-binding domain of the hemagglutinin. Amantadine resistance was detected in 431 of 687 (62.7%) and 0 of 745 (0.0%) of the A(H1N1) viruses from the 2007-2008 and 2008-2009 seasons, respectively.

symmetrel tablets 2017-08-17

Amantadine hydrochloride (Symmetrel), which is an antiviral agent marketed for the prevention of infection by influenza virus, inhibits the mitogenic response of human lymphocytes stimulated with phytohemagglutinin. The concentrations which effectively inhibited the response to phytohemagglutinin were similar to those which Cytoxan And Alcohol maximally inhibit virus replication. The drug inhibited the mitogenic response without affecting the ability of phytohemagglutinin to agglutinate leukocytes. The data suggest that phytohemagglutinin, amantadine, and certain lipid-containing RNA viruses take part in cell-membrane interactions of common nature.

symmetrel medication identification 2017-06-01

M2 proton channel of Parlodel Drug Classification H1N1 influenza A virus is the target protein of anti-flu drugs amantadine and rimantadine. However, the two once powerful adamantane-based drugs lost their 90% bioactivity because of mutations of virus in recent twenty years. The NMR structure of the M2 channel protein determined by Schnell and Chou (Nature, 2008, 451, 591-595) may help people to solve the drug-resistant problem and develop more powerful new drugs against H1N1 influenza virus.

symmetrel reviews 2015-11-09

At month 6, HCV RNA-negative patients made up 54.2% of the interferon + amantadine group and 42.0% of the monotherapy group (P = 0.07). At month 12, HCV RNA-negative patients made up 38.5% of the interferon + amantadine group and 28.4% of the monotherapy group (N.S.). The sustained virological response rates were 21.6% and 20.9%, Dydrogesterone Duphaston Medicine respectively (N.S.).

symmetrel syrup 2017-10-14

Highly pathogenic avian influenza (HPAI) H5N1 virus continues to undergo substantial evolution. Emergence of antiviral resistance among H5N1 avian influenza viruses is a major challenge in the control of pandemic influenza. Numerous studies have focused on the genetic and evolution dynamic of the hemagglutinin and neuraminidase genes; however, studies on the susceptibility of HPAI H5N1 viruses to amantadine and genetic diversity of the matrix (M) gene are limited. Accordingly, we studied the amantadine susceptibility of the HPAI H5N1 viruses isolated in Egypt during 2006-2015 based on genotypic and phenotypic characteristics. We analyzed data on 253 virus sequences and constructed a phylogenetic tree to calculate selective pressures on sites in the M2 gene associated with amantadine-resistance among different clades. Selection pressure was identified in the transmembrane domain of M2 gene at positions 27 and 31. Amantadine-resistant variants emerged in 2007 but were not circulating between 2012 and 2014. By 2015, amantadine-resistant HPAI H5N1 viruses re-emerged. This may be associated with the uncontrolled prescription of amantadine for prophylaxis and control of avian influenza infections in the poultry farm sector in Egypt. More epidemiological research is required to verify this observation.