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Symmetrel (Amantadine)

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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.


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.


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.


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


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.


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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Amantadine and rimantadine have comparable efficacy and effectiveness in relieving or treating symptoms of influenza A in healthy adults, although rimantadine induces fewer adverse effects than amantadine. The effectiveness of both drugs in interrupting transmission is probably low. Routine use of both drugs should be discouraged and both drugs should only be used when all other measures fail.

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A paranoid schizophrenic patient developed the neuroleptic malignant syndrome after receiving three doses of fluphenazine HCl and two doses of thioridazine while he was recovering from major trauma. Treatment with diphenhydramine and benztropine mesylate was ineffective. Administration of amantadine HCl resulted in resolution of all symptoms within 24 hours. After 2 days, the amantadine was discontinued. The following day, the neuroleptic malignant syndrome appeared. Readministration of amantadine again resulted in prompt remission of symptoms.

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Persistent hiccups may have a considerable impact on general health through disturbance of diet, sleep, and mood. They can cause exhaustion, malnutrition, dehydration, wound dehiscence, and even death in extreme cases. We report a complex clinical case of intractable hiccups in a patient with cancer of the pancreas and Parkinson's disease and some of the problems encountered when attempting symptom control. We also discuss a potential therapeutic response to a novel agent, amantadine, unlicensed in the treatment of hiccups.

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Two amino derivatives of (D3)-Trishomocubanes recently synthesized were evaluated for their in vivo and in vitro activities against selected viruses. Both these derivatives exhibited promising in vivo activity against Herpes simplex Type II and Influenza A2/Taiwan, comparable with aciclovir and amantadine, respectively. No in vitro activity was observed for both compounds against Herpes simplex Types I and II and Rhinovirus 1A.

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Animal models in behavioral pharmacology can be evaluated based on their face, predictive and construct validity. A further level of validity may be achieved if a model is reproduced precisely across species--from laboratory animal to human--using identical conditions and manipulations to elicit identical behavioral changes. Under circumstances in which a model achieves 'homologous' validity, it should be possible to demonstrate that the same pharmacological agents produce parallel changes in the same behavior (as distinct from the clinical condition that the animal behaviors are hypothesized to model), when studied in laboratory animals and in humans. Studies have demonstrated that the disruption of sensorimotor gating of the startle reflex, measured by prepulse inhibition (PPI), in rats by dopamine agonists exhibits face, predictive and construct validity for the relative loss of PPI in schizophrenia patients. To assess the homologous validity of this model, and to expand its utility in understanding the pathophysiology of sensorimotor gating deficits and in developing novel antipsychotic agents to reverse these deficits, it will be important to study PPI across species, comparing response profiles to identical pharmacological manipulations. In the present studies, we report that PPI in rats is reduced in a dose-dependent manner by four dopamine agonists that can be administered with relative ease to humans. We also report that the PPI-disruptive effects of the clinically useful dopamine agonist pergolide are reversed by both typical and atypical antipsychotics. These studies establish a foundation for pursuing human pharmacological studies of PPI, and for extrapolating the substantial neurochemical and neurophysiological information from animal studies of PPI, towards understanding the neural basis for deficient sensorimotor gating in specific neuropsychiatric disorders.

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Amantadine, administered at a dose of 200 mg/day, antagonized the extapyramidal symptomatology induced by neuroleptic drugs in fifteen psychiatric patients. Steady-state levels were reached within 4-7 days of treatment. Individual plasma levels ranged from 200-900 ng/ml. Apparent plasma half-lives varied from 10-28.5 h with an apparent VD of 200-400 litres. A significant relationship was found between the plasma levels of amantadine and the effects on the extrapyramidal symptomatology. The data suggest a direct effect of amantadine on dopaminergic receptors.

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HBV RNA is present in virions in plasma specimens from patients with CHB. HBV RNA levels vary significantly from those of established viral markers during antiviral treatment, which highlights its potential as an independent marker in the evaluation of patients with CHB.

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The aim of the study was to evaluate the efficacy of triple antiviral therapy with interferon, ribavirin, and amantadine in comparison with interferon and ribavirin combination treatment in patients with interferon-nonresponsive chronic hepatitis C. We performed an open-label, prospective randomized controlled trial at a secondary referral center. We used a 2:1 ratio, patients received interferon, ribavirin, and amantadine, or interferon and ribavirin for 12 months, and were followed up for an additional 6 months. Ninety-four consecutive adult interferon nonresponders with chronic hepatitis C were screened. Sixty consecutive elected patients entered the study. No patients withdrew because of adverse effects. Forty patients received interferon alfa (5 megaunits on alternate days), ribavirin (800-1,000 mg daily), and amantadine (200 mg daily) for 12 months, and 20 patients received the same treatment without amantadine. At the end of follow-up, alanine transaminase (ALT) level normalization was maintained in 23 of 40 patients (57%) after triple therapy, but in 2 of 20 patients (10%) after double therapy (P <.001, RR = 2.11, 95% CI, 1.43-3.12), whereas disappearance of serum HCV RNA persisted in 19 of 40 patients (48%) and in 1 of 20 patients (5%), respectively (P <.001, RR = 1.81, 95% CI, 1.32-2.47). The safety profile was similar in the 2 groups. In conclusion, in patients with interferon-nonresponsive chronic hepatitis C, triple antiviral therapy for 1 year results in a high rate of sustained biochemical and virologic responses.

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We performed an updated meta-analysis of randomized controlled trials of combination therapy with cholinesterase inhibitors and memantine in patients with Alzheimer's disease.

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In a randomised double blind parallel-group study in three centers budipine, a diphenylpiperidin derivate, was compared to amantadine with respect to efficacy and safety in the monotherapy of mild to moderate Parkinson's disease (PD). From 53 patients of either sex 27 patients were randomised to 3 x 20 mg/d budipine and 26 patients to 3 x 100 mg/d amantadine. The duration of treatment was 4 weeks in 1 center (21 patients) and 12 weeks in the other 2 centers (32 patients). Safety was measured by vital signs, ECG, adverse event recording and clinical laboratory. Both drugs caused a clinically relevant and statistically significant (p < 0.001) improvement of Parkinsonian symptoms according to the Webster-Rating-Scale (WRS) as compared to pretreatment values. With respect to the total WRS score sum there was no difference between the groups (p > 0.05; n.s.), while budipine showed a significantly (p < 0.05) better effect on the main symptom tremor after 12 weeks. During amantadine treatment more adverse events were observed than after budipine intake. Two patients left the study prematurely, one in the amantadine group due to psychiatric adverse events and one in the budipine group because of insufficient efficacy.

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The mean age was 57.4 years (range: 47-72) and the mean disease duration was 30.8 months (range: 11-79). The ataxia severity significantly decreased after intravenous amantadine therapy from 42.5 to 37.3 (p < 0.001). The mean patient global impression scale for improvement was 2.9 and there were no side effects of intravenous amantadine treatment observed. When we assessed responders, the duration of intravenous amantadine effect was more than 1 month in 4 subjects of 7 responders.

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NB is short auxiliary protein with ca. 100 amino acids, encoded in the viral genome of influenza B. It is believed to be similar to M2 from influenza A and Vpu from HIV-1 in that it demonstrates ion channel activity. Channels formed by the protein can be blocked by amantadine. We have synthesized the putative transmembrane segment of NB (IRG S20 IIITICVSL I30 VILIVFGCI A40 KIFI (NB, Lee)). Reconstituted in a lipid bilayer, the peptide shows channel activity. The addition of amantadine leads to dose-dependent loss of channel activity. Channel blocking is reversible. Channel behaviour of the peptide in the presence of amantadine is in accordance with findings for the intact channel. Thus, the synthetic transmembrane peptide captures the ion channel activity of the intact NB protein.

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Randomised controlled trials (RCTs) or quasi-RCTs comparing amantadine and/or rimantadine with no intervention, placebo, other antivirals or different doses or schedules of amantadine or rimantadine in children and the elderly with influenza A.

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In 13 of 27 cases of persistent dyskinesia, treatment with amantadine, in an average dose of 300 mg, brought good to moderate improvement. In 14 patients who showed no response whatever, further treatment, with bromocriptine in doses raised gradually to a final daily dosage of 15 mg, was effective in four cases, though the improvement was generally only moderate. In more than 50 percent of the cases of initial tremor induced by lithium therapy, oxprenolol in daily doses of 160--240 mg produced good effects and moderate improvement was noted in a few further cases. In a series of 20 patients with initial tremor due to neuroleptic therapy, on the other hand, the same treatment proved unsuccessful in the majority of cases. This is the converse of the experience gained with the classical antiparkinson agents, which have proved more effective against tremor induced by neuroleptics than against lithium-induced tremor.

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We searched the Cochrane Acute Respiratory Infections Group Specialised Trials Register, the Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, and the GlaxoSmithKline Clinical Trials Register, generally from inception through to December 2002. We also screened the references of retrieved articles and scrutinised relevant web sites. We also screened references of retrieved articles and other systematic reviews, scrutinised web sites of European and US regulatory bodies, and contacted manufacturers and authors.

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An altered glutamatergic transmission within the central nervous system is supposed to be involved in the generation and propagation of neuropathic pain. Results from experimental studies with animal models of neuropathic pain demonstrate that glutamate antagonists have a positive effect on various parameters. Clinical studies with the NMDA-receptor antagonists ketamine, amantadine, memantine and dextromethorphan and with the antiepileptics gabapentin and lamotrigine, which reduce presynaptic release of glutamate,have been performed. They have shown that most of these substances can reduce neuropathic pain. Important side effects of the NMDA receptor antagonists are hallucination and agitation, whereas tiredness and dizziness are the ones of the antiepileptics. Till now, glutamate antagonists are not drugs of first choice for the treatment of neuropathic pain. However, they are an effective alternative in case the established drugs are not helpful or are not tolerated well.

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This retrospective multicentric study conducted in seven Italian Ambulatory Centers for Dementia assessed the efficacy and safety of memantine 20 mg/day administered for 6 months in addition to an AChEI in AD patients with worsened cognitive functions and behavioral disorders.

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Schizophrenia is comprised of several debilitating symptoms. Antipsychotics offer an effective treatment for positive symptoms, while the negative signs and cognitive deficits are usually treatment-resistant. It was suggested that glutamate dysregulation may be involved in the neuropathology of schizophrenia, mainly through NMDA dysfunction. We hypothesized that addition of memantine, a weak non-selective NMDA receptor antagonist approved for dementia, to antipsychotics would improve the clinical status of un-remitted schizophrenia patients, notably the negative signs and cognitive deficits.

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Chronic ocular hypertension was associated with a reduction in the amplitude of components of the multifocal ERG response and visually-evoked cortical potential. Memantine-treated animals suffered less amplitude reduction for these measures than did vehicle-treated animals, though this treatment effect on the ERG measures was observed only at the early time points (3 and 5 months post IOP elevation). Memantine treatment was not associated with an effect on either the kinetics or amplitude of ERG or VECP response measures obtained from the normotensive eyes.

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Alzheimer's disease (AD) is an age-dependent neurodegenerative disorder and the most common cause of dementia. The early stages of AD are characterized by short-term memory loss. Once the disease progresses, patients experience difficulties in sense of direction, oral communication, calculation, ability to learn, and cognitive thinking. The median duration of the disease is 10 years. The pathology is characterized by deposition of amyloid beta peptide (so-called senile plaques) and tau protein in the form of neurofibrillary tangles. Currently, two classes of drugs are licensed by the European Medicines Agency for the treatment of AD, ie, acetylcholinesterase inhibitors for mild to moderate AD, and memantine, an N-methyl-D-aspartate receptor antagonist, for moderate and severe AD. Treatment with acetylcholinesterase inhibitors or memantine aims at slowing progression and controlling symptoms, whereas drugs under development are intended to modify the pathologic steps leading to AD. Herein, we review the clinical features, pharmacologic properties, and cost-effectiveness of the available acetylcholinesterase inhibitors and memantine, and focus on disease-modifying drugs aiming to interfere with the amyloid beta peptide, including vaccination, passive immunization, and tau deposition.

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We found 19 studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.

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Alzheimer's dementia represents organ failure of the brain. It denotes a clinical milestone that is the result of a pathological process, Alzheimer's disease (AD), which over 1 or more decades has wrought insidious destruction, and finally overwhelmed the brain's capacities to compensate. It is incurable, progressive, and follows an individual pace and course. AD is particularly demanding and devastating to family and caregivers, and patients, all of whom suffer psychologically and emotionally. The cholinesterase inhibitors (ChEIs) donepezil, galantamine, and rivastigmine and the N-methyl- D-aspartate receptor antagonist memantine are approved by the US Food and Drug Administration for AD; they are often used in combination once the disease reaches moderate stages. The relatively good safety profile of these medications, along with their efficacy in alleviating symptoms, is supported by several level-I evidence-grade, short-term, randomized, placebo-controlled trials (RCTs). However, these studies are of limited value in assessing the real-world clinical and economic impact of AD therapies. Long-term, observational studies can provide complementary information to results from short-term clinical trials and more accurately assess practical long-term benefits, risks, costs, and effects on clinically meaningful end points. There is now accumulating and convergent evidence from short- and long-term RCTs, longer-term open-label extensions of RCTs, and long-term observational studies that ChEIs and memantine reduce decline in cognition and daily function, and delay nursing home placement. Optimal care in AD is multifactorial; it includes early diagnosis and multidisciplinary care with educational and nonpharmacological interventions, while ensuring safety, treating comorbidities, caring for caregivers, and appropriate initiation and maintenance of combination therapy.

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Idiopathic spasmodic torticollis (IST) is discussed from the perspective of definition and description, clinical presentation, and modes of treatment including a new, innovative, surgical approach. The role of the physician and the neurosurgical nurse in the management of idiopathic spasmodic torticollis is considered.

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The potential of most N-methyl-D-aspartate antagonists as neuroprotectants is limited by side effects. We previously reported that memantine is an open-channel N-methyl-D-aspartate blocker with a faster off-rate than many uncompetitive N-methyl-D-aspartate antagonists such as dizocilpine maleate. This parameter correlated with memantine's known clinical tolerability in humans with Parkinson's disease. Memantine is the only N-methyl-D-aspartate antagonist that has been used clinically for excitotoxic disorders at neuroprotective doses. Therefore, we wanted to investigate further the basis of its clinical efficacy, safety, and tolerability. Here we show for the first time for any clinically-tolerated N-methyl-D-aspartate antagonist that memantine significantly reduces infarct size when administered up to 2 h after induction of hypoxia/ischemia in immature and adult rats. We found that at neuroprotective concentrations memantine results in few adverse side effects. Compared to dizocilpine maleate, memantine displayed virtually no effects on Morris water maze performance or on neuronal vacuolation. At concentrations similar to those in brain following clinical administration, memantine (6-10 microM) did not attenuate long-term potentiation in hippocampal slices and substantially spared the N-methyl-D-aspartate component of excitatory postsynaptic currents, while dizocilpine maleate (6-10 microM) or D-2-amino-5-phosphovalerate (50 microM) completely blocked these phenomena. We suggest that the favorable kinetics of memantine interaction with N-methyl-D-aspartate channels may be partly responsible for its high index of therapeutic safety, and make memantine a candidate drug for use in many N-methyl-D-aspartate receptor-mediated human CNS disorders.

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Postmortem fluid and tissue concentrations of memantine (Namenda), a drug recently approved for the treatment of Alzheimer's Disease by the FDA, are reported in a suspicious death. In addition, memantine concentrations considered to be incidental findings in three other cases are included to aid in the interpretation in future toxicological investigations. Memantine was extracted from biological samples by a standard liquid-liquid basic drug method followed by analysis utilizing a gas chromatograph-mass spectrometer operated in SIM mode. Blood concentrations ranged from 0.03 to 1.8 mg/L, and the liver concentration was 6.1 mg/kg.

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Levodopa-induced dyskinesias (LID) are amongst the most disabling side-effects of levodopa therapy for Parkinson's disease (PD). It has been suggested that that N-Methyl-D-Aspartate (NMDA)-receptor antagonist may reduce peak-dose dyskinesia in PD patients and may lead to motor improvement. In this study, we compared the efficacy of NMDA receptor antagonists versus placebo in the treatment of LID in PD through a meta-analysis of controlled trials.

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Over the last six years, eight new substances for the treatment of idiopathic parkinsonism (IP) have been approved for use: four oral and one parenteral dopamine agonist (apomorphine), two COMT-inhibitors and budipine. The old drug amantadine has experienced a renaissance in the treatment of a complication occurring during long-term treatment of IP, namely levodopa-induced dyskinesia. Deep brain stimulation with programmable pulse generators and stereotactically implanted electrodes are increasingly being used in patients with severe on-off phases and levodopa dyskinesia. The treatment of Parkinson's disease unresponsive to dopaminergic substances and that associated with dementia remains problematical. In combinations of parkinsonism and dementia, the cholinesterase inhibitors are being used in particular for Lewy body dementia.

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symmetrel dosage 2015-01-07

(1) The anticonvulsant effects of memantine were examined and compared with those of baclofen in monolayer primary cultures of murine nerve cells using conventional intracellular recordings. (2) Memantine and baclofen (each 10-100 microM) decreased spontaneous synaptic activity when action potential frequencies exceeded 6 Hz. Neurons firing action potentials at frequencies below 6 Hz (about 90% of all impaled cells), however, were not affected by the drugs. (3) Memantine reduced the duration of strychnine-elicited bursts and the firing rate of action potentials within a burst. In contrast, baclofen lowered the frequency of the bursts without reducing intra-burst firing. The duration of the bursts was increased. (4) Memantine, but not baclofen, reduced the extent of sustained repetitive firing evoked by pulses of depolarizing current. (5) In the presence of memantine, the second of two electrically evoked action potentials increasingly failed to appear as the intervals between successive stimulating pulses buy symmetrel were shortened. Such an effect was not seen when baclofen was applied. Thus, both antispastic agents, memantine and baclofen, reduce hyperactivity of spinal cord neurons in culture, although their mechanisms of action are different.

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Family physicians should be familiar with the various drugs available for treating and preventing viral infections. Part II of this two-part article focuses on agents used to manage influenza and respiratory syncytial virus. Rimantadine and amantadine traditionally have been used to prevent buy symmetrel and treat influenza type A infections. The neuraminidase inhibitors zanamivir and oseltamivir have a broadened spectrum of activity in the treatment and prevention of influenza types A and B. Ribavirin has been used in some high-risk infants to treat respiratory syncytial virus infections, and palivizumab can be used for prophylaxis.

symmetrel drug summary 2015-01-09

A novel reassortant avian influenza A virus (H7N9) emerged in humans in Eastern China in late February 2013. All virus strains were resistant to adamantanes (amantadine and rimantadine), but susceptible to neuraminidase inhibitors (NAIs) (oseltamivir and zanamivir). One strain (A/shanghai/1/2013) contained the R294K substitution in the neuraminidase (NA) gene, indicating resistance to oseltamivir. buy symmetrel Pyrosequencing has proven to be a useful tool in the surveillance of drug resistance in influenza A viruses. Here, we describe a reverse transcription (RT)-PCR assay coupled with pyrosequencing to identify the NA residues E120, H276, and R294 (N9 numbering) of H7N9 viruses. A total of 43 specimens (26 clinical samples and 17 isolates) were tested. Only one isolate containing the E120V heterogenic mutation was detected by pyrosequencing and confirmed by Sanger sequencing. However, this mutation was not detected in the original clinical specimen. Since virus isolation might lead to the selection of variants that might not fully represent the virus population in the clinical specimens, we suggest that using pyrosequencing to detect NAI resistance in H7N9 viruses directly from clinical specimens rather than from cultured isolates. No cross-reactions with other types of influenza virus and respiratory tract viruses were found, and this assay has a sensitivity of 100 copies of synthetic RNA for all three codons. The high sensitivity and specificity of the assay should be sufficient for the detection of positive clinical specimens. In this study, we provide a rapid and reliable method for the characterization of NAI resistance in H7N9 viruses.

symmetrel drug class 2015-12-09

Systematic reviews of randomized, controlled trials in patients with influenza suggest a buy symmetrel lack of evidence about the effects of antiviral therapy on several patient-important outcomes of influenza.

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Attenuation of the endocrine as well as symptomatic counterregulatory response to recurrent hypoglycaemia is not prevented by the NMDA receptor blocker memantine. Our results buy symmetrel do not support the view that adaptation to repeated hypoglycaemia relies on NMDA receptor-mediated plastic processes involving long-term potentiation or depression.

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The positive effect of bromantan (0.5-50 mg/kg) on the efficiency of physical work of mice and rats (swimming test, running on a treadmill) exceeds that of phenamine administered in optimal doses by 1.3-1.6 times. Such an effect of bromantan lasts no less than 24 h. The drug delays decrease of physical efficiency and restores it sooner in repeated extreme running loads, prevents in rats the corresponding electron-microscopic changes in the cardiomyocyte and buy symmetrel myocyte mitochondria of the skeletal muscles. The data obtained suggest that the positive effect of bromantan on the physical efficiency is associated not only with its psychostimulating action but also with the membrane-protecting effect.

symmetrel generic name 2015-12-09

Pro-cognitive agents for chronic psychotic disorders (CPDs) might buy symmetrel be detected via experimental medicine models, in which neural targets engaged by the drug predict sensitivity to the drug's pro-cognitive effects.

symmetrel syrup 2016-06-28

A total of buy symmetrel 451 patients were treated with memantine (initiated at 5 mg/day and up-titrated with 5 mg weekly to a final dose of 20 mg/day) for 12 weeks. The study endpoints comprised changes from baseline in the scores of the ROSA, ADAS-cog, SIB, DAD, and NPI as well as global changes on the Clinical Global Impression of Change (CGI-C). Analyses were performed for the overall population and by AD severity stage (early, middle, late).

symmetrel 200 mg 2016-09-18

To buy symmetrel define clinical features of patients with alternating hemiplegia of childhood.

symmetrel medication cost 2017-01-02

The mean change from baseline in SIB-L score at week 12 and weeks 24/28 (study end) significantly favored Memantine over placebo treatment (P < .0001 and P = .0182, respectively). Overall, more Memantine-treated patients than placebo-treated patients benefited from treatment. The effect was especially pronounced in patients with substantial language impairment on the SIB-L (baseline score, buy symmetrel treated patients experienced a clinically relevant improvement (25.4% vs. 10.8%, P = .0414), and significantly fewer patients experienced clinically relevant worsening (32.8% vs. 60.0%, P = .0029).

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At the end of treatment, 5 (33.3%) patients responded to the combination therapy, and 7 (46.7%) patients responded to interferon therapy alone. Twelve months after cessation of the treatment, 3 (21.4%) patients had a buy symmetrel sustained complete response to the combination therapy, and 3 (20.0%) patients had a sustained complete response to interferon alone (P = 0.64).

symmetrel en alcohol 2016-12-12

The synthesis of some spiro[cyclopropane-1,2'-adamantan]-2-amines and methanamines and some spiro[pyrrolidine-2,2'-adamantanes] is described. The title compounds were evaluated against a wide range of viruses (influenza A, influenza B, parainfluenza 3, RSV, HSV-1, TK- HSV-1, HSV-2, vaccinia, vesicular stomatitis, polio 1, coxsackie B4, sindbis, semliki forest, Reo 1, HIV-1, and HIV-2), and some of them (compounds 6b, 6c, 9a, 16a, 16b, and 17) inhibited the cytopathicity of influenza A virus at a concentration significantly lower than that of amantadine and also significantly lower than the concentrations buy symmetrel at which they proved cytotoxic to the host cells. None of the new aminoadamantane derivatives was active against influenza B virus or any of the other viruses tested, which points to their specificity as anti-influenza A virus agents.

symmetrel medication 2016-03-06

Our randomized pilot study, though small, clearly indicates that interferon alfa-induced depressive symptoms can be prevented by the use of amantadine. However, double buy symmetrel -blind placebo-controlled trials with a higher sample size are required to confirm these preliminary findings.

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Twenty-one adults who had gained at least 5 lb with olanzapine were randomly assigned to receive amantadine (N=12) or placebo (N=9) in addition to olanzapine. The length of time taking olanzapine buy symmetrel ranged from 1 to 44 months. Body mass index, psychiatric status, and fasting blood levels were assessed at baseline and 12 weeks.

symmetrel generic 2017-04-30

The experiments on rats showed for bemithyl LD50 = 581.48 ( Indocin Dosage 350.17-965.57) mg/kg and for bromithyl LD50 = 1750.30 (1463.07-2093.92) mg/kg (males) and 1584.29 (1280.46-1960.22) mg/kg (females). The therapeutic ratios are 4-6 for both drugs, while the toxicity index is 10-15 for bemithyl and 20 <196> 22 for bromithyl. It was established that ergotropic effects prevail in the toxicity of bemithyl administered in the 20-80 mg/kg dose range, while trophotropic effects are dominating at doses above 100 mg/kg. Bromithyl exhibits a dose-dependent trophotropic effect in the entire dose range.

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Memantine is an N-methyl-D: -aspartate (NMDA) receptor antagonist, approved for the treatment of moderate to severe Alzheimer's disease (AD). We conducted a 4-month observational, post-marketing, Austrian study of memantine in 377 outpatients with moderate to severe AD. In this 'real-life' setting, memantine was well-tolerated, and produced benefits in cognition (Mini-Mental State Examination), activities of 4 Mg Lexapro daily living (Activities of Daily Living score), and global function (Clinical Global Impression scale). Treatment effects were apparent in both pre-treated and treatment-naïve patient subgroups.

symmetrel drug classification 2015-01-03

This was a retrospective cohort study examining maternal and neonatal outcomes after antepartum exposure to antiviral therapy for influenza. We evaluated maternal characteristics, pregnancy outcomes, and fetal outcomes and compared them with our overall Imitrex Dosage Injection obstetric population.

symmetrel 100 mg 2015-12-16

In a double-blind placebo-controlled crossover study of ten patients with multiple sclerosis, we found amantadine hydrochloride therapy to be effective in improving fatigability in six. Administration of the drug was associated with significantly higher levels of beta-endorphin-beta-lipotropin and responders had significantly higher levels than nonresponders. Lactate levels were significantly higher and pyruvate levels Risperdal Good Reviews lower in nonresponders. Amantadine given for fatigue to patients with multiple sclerosis is associated with measurable changes in levels of metabolites and peptides in the circulation.

symmetrel reviews 2016-08-23

Amantadine has been used Aggrenox Generic Brand since 1969 in the treatment of Parkinson's disease. In 1970, were described the special symptoms noted in the lower limbs due to this drug. The authors, after a review of the various disturbances, have studied 10 cases by Capillaroscopy. They emphasize the interest of the study of this abnormality of the micro-circulation, producing vaso-constriction of the arterioles and venules.

symmetrel drug interactions 2016-11-23

A growing body of literature implicates interactions between glutamatergic and neostriatal dopaminergic Celebrex 20 Mg neurotransmitter systems in the development and expression of impulsivity, hyperactivity, and stereotypy. Amantadine hydrochloride, a drug used in young children for influenza prophylaxis, acts both as an indirect dopamine agonist as well as an N-methyl-D-aspartate (NMDA) receptor antagonist. Thus an open clinical trial of this medication for the treatment of symptoms of impulse control disorders in children was performed.

symmetrel user reviews 2017-12-07

Four hundred fifty volunteers participated in a placebo-controlled, double-blind, randomized trial of the prophylactic effects of rimantadine and amantadine during Hytrin Bph Dose an outbreak of influenza A. The subjects received drugs orally at a dose of 100 mg twice a day for six weeks. Influenza-like illness occurred in 41 per cent of the subjects receiving placebo but in only 14 per cent of those receiving rimantadine and 9 per cent of these receiving amantadine (P less than 0.001 for either drug vs. placebo). Laboratory-documented influenza occurred in 21 per cent of placebo recipients, 3 per cent of rimantadine recipients, and 2 per cent of amantadine recipients (P less than 0.001). These findings represent efficacy rates of 85 per cent for rimantadine and 91 per cent for amantadine, as compared with placebo. More recipients of amantadine (13 per cent) than recipients of rimantadine (6 per cent; P less than 0.05) or placebo (4 per cent; P less than 0.01) withdrew from the study because of central-nervous-system side effects. On the basis of this study, rimantadine appears to be the drug of choice for the prophylaxis of influenza A.

symmetrel dosage forms 2017-06-06

Less than half of the AD patients in nursing homes receive ChEls or memantine and approximately one third of the residents could possibly qualify for Zovirax 100 Mg reimbursement. Many residents with cognitive deficits remain undetected and undiagnosed and consequently do not receive appropriate treatment.

symmetrel overdose 2016-01-20

Neurotoxicological profile of actoprotector bromantane was studied on rats using S. Irwin's protocol of multi-test observation. The drug in doses of 30-300 mg/kg stimulated and in doses of 600-9,600 mg/kg suppressed behavioral activity. Spontaneous motor activity increased after single treatment with bromantane in doses of 30-300 mg/kg, did not change after treatment in doses of 600 mg/kg, and was inhibited after treatment in doses above 600 mg/kg. In doses of 300-600 mg/kg the drug reduced pain sensitivity threshold and in doses above 600 mg/kg elevated the pain threshold and tactile sensitivity and reaction to knock. Bromantane induced mydriasis in all studied doses; in doses above 10 g/kg the preparation induced blepharoptosis. In doses above 5 g/kg bromantane slightly increased respiration rate and depth (Kussmaul-like respiration). In some animals bromantane in high doses induced regurgitation, diarrhea, and polyuria. Rectal temperature decreased by 0.5-1 degrees C after virtually all doses. Behavioral effects of bromantane in doses of 30 and 600 mg/kg were associated with stimulation of Parlodel Reviews the central dopamine and suppression of muscarinic and nicotinic cholinergic structures, n-cholinolytic effects of bromantane was more pronounced at a dose of 30 mg/kg than at a dose of 600 mg/kg.

symmetrel 100mg capsules 2017-08-25

Severity ofprecipitated Ventolin Y Alcohol opioid withdrawals.

symmetrel medication identification 2015-07-01

Chemotherapy for patients chronically infected with hepatitis C virus (HCV) is ineffective in over 50% of cases, generating a high demand for new drug targets. The p7 protein of HCV displays membrane channel activity in vitro and is essential for replication in vivo though its precise role in the virus life cycle is unknown. p7 channel activity can Himalaya Vasaka Capsules be specifically inhibited by several classes of compounds, making this protein an attractive candidate for drug development, though techniques used to date in characterising this protein are unsuited to compound library screening. Here we describe an assay for the channel forming ability of p7 based on the release of a fluorescent indicator from liposomes. We show that recombinant p7 from genotype 1b HCV causes a dose-dependent release of dye when mixed with liposomes and that this property is enhanced at acidic pH. We demonstrate that this activity is due to the formation of a size-selective pore rather than non-specific disruption of liposomes and that activity can be blocked by amantadine and several other compounds, validating it as a measure of p7 channel function. This system provides the first convenient in vitro assay for exploiting p7 as a therapeutic target.

symmetrel brand name 2017-11-24

A prospective examiner-blind, cross-over study was conducted to compare the efficacy of memantine (40 or 60 mg/day) and gabapentin (1,200 mg/day) as therapy for acquired fixational pendular nystagmus (APN) in 11 patients with multiple sclerosis. APN was documented in 20 eyes by electrooculography (EOG). The primary objective of the study was an at least 50% reduction in amplitude and/or frequency of APN compared with baseline values in EOG. This aim was reached for 17 of 20 APN-affected eyes with memantine 40-60 mg and for 11 eyes with gabapentin up to 1,200 mg. A complete cessation of APN was achieved in eight eyes (four patients) with memantine 40 mg and in a further four eyes (two patients) with memantine 60 mg. One patient achieved the same benefit with memantine 40 mg and gabapentin. In two other eyes APN completely subsided with gabapentin 1,200 mg only, but not with memantine. Near visual acuity, a secondary outcome parameter, improved by at least 0.1 in 11 of 17 eyes treated with memantine and in 8 out of 16 eyes treated with gabapentin. In summary, memantine and gabapentin are safe and effective treatment options for APN.

symmetrel pill 2017-07-07

There is little knowledge regarding the underlying mediating factors for cognitive control at the synaptic level, especially the role played by glutamatergic neurotransmission. In the current study the effect of the NMDA receptor antagonist memantine was examined in a pharmacological fMRI study. Thirty-one healthy adults were scanned twice in a counter-balanced design, either drug naïve or after administration of memantine for 21 days, to build up a steady-state plasma concentration in all participants. The participants performed an auditory attention control task while in the MR scanner. The results showed significant reduction in activation in prefrontal cortex and anterior cingulate cortex after memantine administration compared to the drug naïve session. We suggest that the present results may have implications for the understanding of deficits in cognitive control in psychiatric disorders, like schizophrenia, through altered glutamatergic neurotransmission.