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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.

symmetrel en alcohol

Glutamate is a major neurotransmitter in the central nervous system (CNS). Large amount of glutamate can overstimulate N-methyl-D-aspartate receptor (NMDAR), causing neuronal injury and death. Recently, NMDAR has been reported to be found in the lungs. The aim of this study is to examine the effects of memantine, a NMDAR channel blocker, on bleomycin-induced lung injury mice.

symmetrel reviews

Young onset Parkinson's disease (YOPD) is defined as idiopathic Parkinson's disease (IPPD) occurring in people between 21 and 40 years of age; it strikes approximately 5% of Parkinson's patients. YOPD has earlier onset of motor complications than later onset Parkinson's disease. Motor complications and disease progression are responsible for devastating morbidity. Current medical and surgical treatments can dramatically ameliorate motor complications and help maintain function and employment. Patient education, support, and advocacy provided by nursing staff can influence the treatment options for these patients, having a significant effect on the future course of the disease. This case history documents the course of a YOPD patient with unusually severe motor complications. He is the only patient at Puget Sound Neurology ever to develop rhabdomyolysis due to dyskinesias. Following bilateral subthalamic nucleus deep brain stimulation, his Parkinson's symptoms have improved dramatically, and his motor complications are significantly improved.

symmetrel medication identification

Dopaminergic drug treatment is persistently reduced and simplified following chronic STN-DBS for up to 3 years.

symmetrel generic name

Catatonia, originally described by Karl Kahlbaum in 1874, may be regarded as a set of clinical features found in a subtype of schizophrenia, but the syndrome may also stem from organic causes including vascular parkinsonism, brain masses, globus pallidus lesions, metabolic derangements, and pharmacologic agents, especially first generation antipsychotics. Catatonia may include paratonia, waxy flexibility (cerea flexibilitas), stupor, mutism, echolalia, and catalepsy (abnormal posturing). A case of catatonia as a result of acute renal failure in a patient with dementia with Lewy bodies is described. This patient recovered after intravenous fluid administration and reinstitution of the atypical dopamine receptor blocking agent quetiapine, but benzodiazepines and amantadine are additional possible treatments. Recognition of organic causes of catatonia leads to timely treatment and resolution of the syndrome.

symmetrel drug summary

The treatment of two cases of Creutzfeldt-Jakob disease with amantidine is described. The first case made a remarkable initial improvement which was sustained for two months, but then deteriorated and died. Histological examination of the brain showed changes consistent with early Creutzfeldt-Jakob disease. The second case which was clinically one of Creutzfeldt-Jakob disease has now been followed for 30 months since the start of treatment and appears to be cured. It is considered that amantidine has a definite effect in this disease and it is suggested that its mode of action, though unknown, is more likely to be metabolic than antiviral.

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To review the first generation of antiviral agents (e.g., idoxuridine, amantadine, vidarabine) that paralleled discovery of antineoplastic agents.

symmetrel medication

After a patient is diagnosed with Parkinson disease (PD), there are many therapeutic options available. This article provides examples of prototypical patients encountered in clinical practice and illustrates the various pharmacologic and nonpharmacologic treatment options for the motor symptoms of PD.

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Glutamate is the major transmitter candidate between inner hair cells and the afferent neurons of the mammalian cochlea. We investigated the action of memantine (1-amino-3,5-dimethyl-adamantane) and the quinoxaline derivative caroverine [1-diethylaminoethyl-3,8-(p-methoxybenzyl)-1,2-dihydro-quinoxaline-dione] on the glutamatergic transmission in the guinea pig cochlea utilizing extracellular recording techniques and microiontophoretic ejection of substances. While memantine was able to inhibit the NMDA (N-methyl-D-aspartate)-induced firing, the AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid)-stimulated activity was unaffected. In contrast, caroverine could block both NMDA- as well as AMPA-induced firing. As memantine and caroverine are currently in clinical use, these substances could be introduced to the treatment of several cochlear disorders.

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Outpatients with MCI and AD in ADNI.

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In this population, concomitant memantine use did not alter the response profile of donepezil 23 vs. 10 mg/day. Donepezil 23 mg was generally safe and well tolerated among patients receiving donepezil alone and among patients receiving a combination of donepezil and memantine therapy.

symmetrel dosage forms

In cases of corneal edema and in the absence of any identifiable ocular causes, a review of toxic effects of systemic medication should be undertaken. Amantadine can cause corneal decompensation and needs to be considered as part of the differential diagnosis of corneal edema.

symmetrel drug

Memantine, a NMDA receptor antagonist used in several experimental models of neuronal cell injury, is a neuroprotective agent that can attenuate neuronal apoptosis connected with over-stimulation of NMDA receptors. In the present study, we evaluated the impact of memantine on apoptosis in primary cerebellar granule cell (CGC) cultures at 7 and 12 day in vitro (DIV). Cell death was induced by staurosporine (St, 0.5 microM) or by decreasing the level of potassium in the culture medium (LP, 5 mM KCl). Both treatments induced cell death in CGC with higher cell-damaging effects at 12 DIV and 7 DIV neurons for St and LP, respectively. Memantine (0.1-2 microM) partially attenuated St-induced apoptosis only in 7 DIV CGC as assessed by DNA fragmentation and LDH release, but not caspase-3 activity. During LP-induced apoptosis, memantine decreased LDH release and DNA fragmentation, but not affected caspase-3 activity in 7 and 12 DIV CGC. Interestingly, we found no beneficial effects of other NMDA antagonists, including a competitive antagonist such as AP-5 (100 microM) and an uncompetitive antagonist such as MK-801, (1 microM). In conclusion, our data suggest that the anti-apoptotic effects of memantine in CGC are developmentally regulated and its neuroprotective action occurs through an NMDAR-independent mechanism.

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Rates of change were modeled using trial and registry-based patient level data. A discrete event simulation projected outcomes for three identical patient groups: donepezil 10 mg, memantine 20 mg and no therapy. Patient mix, mortality and costs were developed using Germany-specific sources.

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A group of 27 patients with Friedreich's ataxia and another group of 30 patients with olivopontocerebellar atrophies were each randomly divided into two subgroups, one receiving placebo and the other amantadine hydrochloride (AH; 200 mg daily) for three to four months.

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In vivo pulse voltammetry was used to study the effect of anti-parkinsonian drugs and of neurotoxins in rat striatum. It could be demonstrated that besides the well-known changes of total dopamine (DA) concentrations the applied drugs affected also the extraneuronal DA metabolism in the living rat. In addition, neurotoxin-treated rats can be used as a model to study some aspects of the Parkinson syndrome.

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Memantine, a non-competitive antagonist of NMDA receptors, has recently been used in Alzheimer's disease. The influences of memantine on behavioral changes, monoamine oxidase (MAO) activity and reuptake of both serotonin (5-HT) and dopamine in mice were examined in the present study. Memantine dose-dependently increased locomotor activity. This effect was inhibited by intraperitoneal (i.p.) administration of haloperidol. Furthermore, administration [intracerebroventricular (i.c.v.)] of memantine did not induce the head-twitch response (HTR). However, the 5-HT-induced HTR was potentiated by the combined administration of memantine. The enhanced HTR was inhibited by i.p. administration of haloperidol or 5-HT(2A) antagonist ketanserin. Memantine at 1 mM inhibited both MAO-A and MAO-B activities in mouse forebrain homogenates to 37% and 64% of controls, respectively. Lineweaver-Burk plots analysis revealed competitive inhibition with both MAO-A and MAO-B. The inhibitions were also reversible. Memantine inhibited the reuptake of both 5-HT and dopamine into mouse forebrain synaptosomes. 5-HT and dopamine reuptakes were inhibited to 2% and 16% of controls, respectively, with 1 mM memantine. These findings suggest that the increased locomotor activity and enhanced 5-HT-induced HTR by memantine may result from the reuptake and turnover inhibitions of 5-HT and dopamine.

symmetrel drug classification

Nosocomial transmission of influenza has been reported infrequently; however, patients in general hospitals are often among the most susceptible to the complications of influenza infection. Hospital-acquired influenza may occur more often than is reported, but it may be recognized because of lack of diagnostic facilities or the time required for virus isolation and identification. Based on the mode of transmission in the hospital, the established reservoirs of influenza virus, and duration of virus shedding, isolating patients with influenza may occasionally be useful but restricting visitors is probably not required. Vaccinating hospital personnel with influenza vaccine and, if influenza A is prevalent, giving amantadine hydrochloride to high-risk patients or personnel should both be considered.

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A sustained virological response (SVR) was shown in 31.8% (seven of 22 patients). With the naïve patients, the SVR rate was 21.4% (three of 14 patients). In patients who could not eradicate HCV-RNA by previous IFN monotherapy, the SVR rate was 50% (four of eight patients).

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At the end of the 2003-4 influenza season, we conducted a cross sectional on-line survey of physician knowledge, attitudes and practices regarding rapid diagnostic testing and use of antiviral therapy for influenza at two large academic medical centers, one in Massachusetts and the other in Texas. We collected data on self-reported demographics, test use, prescribing practices, and beliefs about influenza and anti-influenza drugs.

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High-level evidence related to pharmacological strategies for managing Lewy body dementia is rare. Strategies for important areas of need in Lewy body dementia, such as autonomic symptoms and caregiver burden, have not been investigated, nor have the views of patients and caregivers about pharmacological strategies.

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The antiviral effect of amantadine (1-aminoadamantane) was tested in vitro as well as in vivo. Treatment of persistently Borna disease virus (BDV)-infected cell lines of different origin and for various length of time did not result in a general reduction of virus titer or clearance of virus from infected cells. In vivo, rats were treated with amantadine by daily oral application or by use of osmotic pumps, and in both cases treatment was started before infection. Neither route of application of the drug had any influence on the time of onset of disease, on antiviral antibody titers, on virus titer in the brain, on the severity of the inflammatory reaction in the brain, or on the severity of neurological symptoms. These experiments, although revealing negative results and obtained using a virus from a natural case of Borna disease grown after isolation in vitro for a long period of time, should caution from the general use of amantadine as a curative agent against BDV infection as has been implicated recently [Bode et al. (1997) Lancet 349:178-179].

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A full comparison of the satisfaction with treatment using the current Alzheimer's disease (AD) therapies from the perspective of caregivers has not yet been done. The aim of this study was thus to find out the degree of satisfaction with the main available drug treatments in monotherapy for AD from this point of view.

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symmetrel dosage 2016-02-02

The recognition of viruses as causes of pneumonia in both immunocompetent and immunocompromised hosts has expanded dramatically. The number of therapeutic agents available for treatment of these illness also has increased in the last decade. Each of these agents has demonstrated a limited therapeutic indication for treatment of viral pneumonia. Many of these agents inhibit viral DNA synthesis through actions as nucleoside analogs (such as acyclovir and ganciclovir). However, a variety of alternative mechanisms of inhibition of viral replication are used. Ribavirin, while being a nucleoside analogue, also appears to exert broad antiviral activity by a variety of enzymatic inhibitory mechanisms. Foscarnet, an inorganic pyrophosphate analogue, offers additional treatment options for herpesviruses by acting as a direct virus DNA polymerase inhibitor. The buy symmetrel online tricyclic amines amantadine and rimantadine inhibit influenza A replication by interfering with viral uncoating after cell penetration. Thus, these two agents are largely effective as prophylaxis. The search for novel antiviral drugs, such as neuraminadases inhibitors with selective influenza activity, is currently in progress.

symmetrel medication identification 2015-08-12

Low doses of N-methyl-D-aspartate (NMDA)-type glutamate receptor antagonists induce morphological alterations in neurons of the cingulate gyrus and retrosplenial cortex of the rat. Neuronal cell death may result at higher doses. These effects are a major concern with regard to the introduction of new NMDA receptor antagonists into clinical trials. Amantadine is an uncompetitive NMDA receptor antagonist, which has been in clinical use for many years. In the present study we have looked for possible morphological alterations like necrosis in postmortem human brain tissue of patients previously treated with amantadine. Formalin-fixed tissue samples were taken from the hippocampus, cingulate gyrus, and retrosplenial cortex of 8 patients on previous amantadine medication and of 11 controls. Histopathological examination of sections was performed blind. All brains except one revealed either nonspecific age-related or cerebrovascular changes or other neurodegenerative disorders including Alzheimer's, Parkinson's or Lewy body disease. In conclusion, histopathological examination of the hippocampus, retrosplenial cortex, and cingulate gyrus of human brain did not reveal changes buy symmetrel online suggested to be specific for previous amantadine treatment.

symmetrel buy 2016-03-07

Two review authors independently extracted data and assessed trial quality buy symmetrel online .

symmetrel pill 2017-04-01

At the end of treatment and after the 24-week follow-up period, serum hepatitis C virus buy symmetrel online RNA was undetectable in eight (53%) and six (40%) patients treated with standard-dosage interferon-alpha, respectively, compared with 11 (73%) and 10 (67%) treated with high-dose interferon-alpha, respectively (not significant). The safety profile of both treatment regimens was similar. Severe adverse events leading to withdrawal from the study occurred in one patient (7%) in each group, and in both groups one patient (7%) was lost during therapy for unknown reasons.

symmetrel cost 2015-01-13

Ethanol blocks N-methyl-d-aspartic acid (NMDA) glutamate receptors. Increased NMDA receptor function may contribute to motivational disturbances that contribute to alcoholism. The authors assessed buy symmetrel online whether the NMDA receptor antagonist memantine reduces cue-induced alcohol craving and produces ethanol-like subjective effects.

symmetrel generic name 2016-03-23

This study supports the theory that amantadine buy symmetrel online might be a powerful antidiabetic tool and could be added to the therapeutic arsenal against type 2 diabetes.

symmetrel 100 mg 2016-10-12

There are buy symmetrel online a number of simple, accurate, and fast tools to facilitate case detection, including the Mini-Mental State Examination. Once a diagnosis has been made, healthcare providers, patients, and caregivers can evaluate treatment options. Several medications are available for symptomatic treatment of AD, including the cholinesterase inhibitors donepezil, galantamine, and rivastigmine, and for later stage disease, the N-methyl D-aspartate (NMDA) receptor antagonist, memantine.

symmetrel tablets 2017-07-10

Treatment with escitalopram (mean daily dose 18.62 mg, SD 5.15) and memantine (mean daily dose 13.62 mg, SD 6.67) was associated with improvement in Hamilton Depression Rating buy symmetrel online Scale scores over the 48-week study period. Patients demonstrated significant improvement in the primary outcome of cognitive performance (Selective Reminding Test total immediate recall; SRT-IR) over the 48-week treatment period (p = 0.0147). Significant improvement was also observed in measures of naming and verbal fluency but not in the other cognitive domains. One of the 35 patients (2.9%) converted to Alzheimer's disease over the 48-week treatment period. In the amnestic mild cognitive impairment subsample (n = 22), the conversion rate was 4.5%, a rate lower than in other reports of patients with DEP-CI.

symmetrel reviews 2015-04-18

Electrophysiological assays on mammalian central neurons in monolayer dissociated cell culture allow classification of clinically used anticonvulsant drugs on a mechanistic basis and predict their clinical spectrum of anticonvulsant efficacy consistently in comparison with data from animal models. Clinical anticonvulsant efficacy of memantine and flunarizine against tonic-donic and partial seizures is predicted on the basis of ability to limit sustained high efficacy frequency repetitive firing of sodium-dependent buy symmetrel online action potentials and to suppress depolarizing burst firing of neocortical, hippocampal and spinal cord neurons in cell culture. Effects on voltage-sensitive sodium channels, and possibly potassium channels, may explain, at least in part, the mechanism of anticonvulsant efficacy of memantine and flunarizine.

symmetrel capsules 2016-01-27

For each group, the duration of fever (i.e buy symmetrel online ., body temperature, > or = 37.5 degrees C) was significantly shorter in patients who received the drug within 12 h after the onset of symptoms than in patients who received the drug > 12 h after the onset. For all 3 groups, the duration of fever was shorter in patients with a highest temperature < 39 degrees C than in patients with temperatures > or = 39 degrees C. The duration of fever was significantly longer for the B+Os group than for the A+Os group. Multiple regression analysis found that the type of influenza, the highest body temperature, and the time between the onset of symptoms and the start of treatment are independent factor that influence the duration of fever.

symmetrel drug classification 2017-07-28

The patients were treated with 20 mg/day of memantine for a 6-month period buy symmetrel online . The efficacy of memantine was evaluated using the Mini-Mental State Examination, the Nurses' Observation Scale for Geriatric Patients (NOSGER) and the Explorationsmodul Demenz (EMD) scale. In addition, a global assessment was made by the physician.

symmetrel medication 2016-02-22

Parkinson's disease (PD) clinical features comprise both motor and nonmotor manifestations. Among the nonmotor complications, dementia is the most important. Approximately 40% of PD patients are affected by cognitive impairment. Remarkably, in addition to age, dementia is an independent predictor of mortality, whereas age at onset of PD and severity of neurological symptoms are not. In this review, I summarize the current knowledge of the pathogenesis of the PD cognitive impairment in relation to the therapies presently accessible and those that could become strategic in the near future. It is hypothesized that patients with PD show two components of cognitive dysfunction (CD): a generalized profile of subcortical dementia (PDsCD), and an overlapped pattern suggesting specific prefrontal damage with CD (PDpFCD). PDsCD is associated with structural neocortical/subcortical changes in the brain (in frontal, parietal, limbic, and temporal lobes, as well as in midbrain structures). In PDpFCD cognitive deficits comprise impairments in neuropsychological tests sensitive for frontal lobe function (discrete elements of episodic and working memory for instance), which are considered to be the consequence of dysfunction in neuronal loops connecting the prefrontal cortex and basal ganglia. Drugs reviewed for targeting PDsCD include: cholinesterase inhibitors, agents with mixed cholinergic and dopaminergic properties, antiglutamatergic drugs, mixed antiglutamatergic/dopaminergic agents; antioxidants and enhancers of mitochondrial functions, and anti-COX-2, as well as other anti-inflammatory mediators. Preliminary studies with vehicles that may target PDpFCD include piribedil, tolcapone, amantadine, and farampator. Additional agents (citicoline and neuroimmuniphilines, among others) will be outlined. A brief overview on neuroprotection and promising new biological advances in PD (deep brain buy symmetrel online stimulation, stem cells, gene therapy) also will be summarized.

symmetrel dosage forms 2017-08-13

A comprehensive systematic search of MEDLINE using focused search criteria, a search of reference lists from these studies and reviews, a review of the Cochrane Database of buy symmetrel online Systematic Reviews, and a hand search of relevant journals was conducted. Selection of articles was based on the clinical focus. Additional inclusion criteria preferentially selected key articles that contained higher-level evidence in accordance with explicit, validated criteria.

symmetrel drug class 2016-05-09

Determine whether memantine improves cognitive buy symmetrel online performance (CP) among subjects with multiple sclerosis (MS) and cognitive impairment (CI).

symmetrel generic 2017-11-07

Pneumonia remains the leading infectious disease-related cause of death among the elderly. Streptococcus pneumoniae is the most frequent pathogen Effexor Overdose Death isolated from aged individuals with community-acquired pneumonia. Other common bacteria that cause this disease include Haemophilus influenzae and Legionella pneumophila. Manifestations of pneumonia in the elderly can be subtle and result in delayed recognition and treatment. Gram stain evaluation and culture of non-contaminated expectorated sputum remain the conventional techniques to guide initial antibiotic selection. While the presence of a new infiltrate on chest X-ray confirms the clinical diagnosis of pneumonia, the radiographic appearance of the infiltrate cannot accurately define the etiologic agent. Specific therapeutic measures include administration of appropriate antibiotics, correction of fluid and electrolyte imbalances, nutritional support and treatment of concomitant disorders. Preventive measures include use of influenza vaccine, amantadine and pneumococcal vaccine.

symmetrel en alcohol 2017-04-26

Twenty patients with idiopathic Parkinson's disease (PD) and motor fluctuations received open-label amantadine (100-200 mg/d) in addition to their other antiparkinson medications. One patient had unpredictable motor fluctuations (on-off Feldene Pain Medication ) and the others had end-of-dose wearing-off. The effect of amantadine on motor fluctuations and parkinsonian disability was tested at 1, 2, and 3 months. Moderate improvement in motor fluctuations occurred in 55% of the patients at 2 months and 65% of patients at 3 months of treatment (p less than 0.01). There was also significant improvement in parkinsonian disability. The duration of improvement averaged 5.7 months, and all patients deteriorated to their baseline level of function within 12 months. This study suggests that the addition of amantadine can transiently improve motor fluctuations and have a significant impact on overall disability in patients with chronic PD.

symmetrel drug summary 2017-09-26

Rodent models of l-DOPA-induced dyskinesia (LID) are essential to investigate pathophysiological mechanisms and treatment options. Ratings of abnormal involuntary movements (AIMs) are used to capture both qualitative and quantitative features of dyskinetic behaviors. Thus far, validated rating scales for the mouse have anchored the definition of severity to the time during which AIMs are present. Here we have asked whether the severity of axial, limb, and orolingual AIMs can be objectively assessed with scores based on movement amplitude. Mice sustained 6-OHDA lesions in the medial forebrain bundle and were treated with l-DOPA (3-6mg/kg/day) until they developed stable AIMs scores. Two independent investigators rated AIM severity using both the validated time-based scale and a novel amplitude scale, evaluating the degree of deviation of dyskinetic body parts relative to their resting position. The amplitude scale yielded a high degree of consistency both within- and between raters. Thus, time-based scores, amplitude scores, and a combination of the two ('global AIM scores') were applied to compare antidyskinetic effects produced by amantadine and by the following subtype-specific DA receptor antagonists: SCH23390 (D1/D5), Raclopride (D2/D3), PG01037 (D3), L-745,870 (D4), and VU6004461 (D4). SCH23390 and Raclopride produced similarly robust reductions in both time-based scores and amplitude Prednisone Safe Dosage scores, while PG01037 and L-745,870 had more partial effects. Interestingly, a novel and highly brain penetrable D4 receptor antagonist (VU6004461) markedly attenuated both time-based and amplitude scores without diminishing the general motor stimulant effect of l-DOPA. In summary, our results show that a dyskinesia scale combining a time dimension with an amplitude dimension ('global AIMs') is more sensitive than unidimensional scales. Moreover, the antidyskinetic effects produced by two chemically distinct D4 antagonists identify the D4 receptor as a potential future target for the treatment of LID.

symmetrel brand name 2017-08-28

Normal rhesus monkey erythrocytes were incubated with various membrane-active drugs (for 1 h at 37 degrees C) and after thorough washing, were exposed to infection with Plasmodium knowlesi in an invitro cultivation system. The ability of merozoites to infect with drug-pretreated erythrocytes was assessed both by counting the number of infected cells and by measuring the incorporation of [3H]isoleucine into parasite protein. Marked inhibition of invasion was observed with vinblastine and colchicine, at concentrations greater than 5 x 10(-4) M, respectively. At similar concentrations, cytochalasin B or amantadine had no apparent effect. The addition of 10(-3) M 3',5'-cAMP to the medium during the incubation in the presence of colchicine or vinblastine partially decreased the inhibitory effects. The effects of colchicine and vinblastine on parasite invasion may be correlated with a reversible alteration in erythrocyte conformation (spherocytosis) which occurs at similar drug concentrations to those above and which Cardura Maximum Dose can be relieved by simultaneous incubation with cAMP. A possible mechanism of action is proposed.

symmetrel medication cost 2016-08-27

The presence of glutamate receptor subunits in two laryngeal cancer cell lines (RK33 and RK45) was evaluated by means of end-point PCR, real-time PCR, and Flomax Drug Uses immunocytochemistry.

symmetrel drug 2015-03-11

The present study investigated the effects of a single oral dose (30 mg) of the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist memantine on memory and learning in human subjects. Sixteen male healthy volunteers participated in a double blind placebo controlled Biaxin Medication study. There were no significant effects of memantine on mood, attention or immediate and delayed verbal and visuospatial memory. Memantine did, however, delay the acquisition of classical eyeblink conditioning and reduced the overall frequency of conditioned responses without affecting reflex or spontaneous eyeblinks. These findings are compatible with the higher affinity of memantine to cerebellar as compared to forebrain tissue and demonstrate the dissociability of different memory systems by pharmacological tools.

symmetrel 100mg capsules 2015-03-19

The antiviral drug amantadine has anticholinergic effects in the guinea-pig atrium at concentrations greater than 1 X 10(-4)M. It is a competitive inhibitor of [3H]-quinuclidinyl benzilate binding to the muscarinic receptor, but antagonizes the negative inotropic effect of acetylcholine in a non-competitive manner. It increases the duration of the atrial action potential and also increases the force of atrial contraction. These effects are evident at approximately 10 times lower concentrations than the antimuscarinic effects. The increase in contractility can be reversed by propranolol (5 X 10(-7)M) but the increase in action potential duration is potentiated by propranolol. Shortening of the action potential duration by acetylcholine was reversed by amantadine, but at approximately ten times lower levels than were needed to reduce the negative inotropic effect. Interactions between beta adrenoceptor binding of [3H]-dihydroalprenolol and amantadine could not be demonstrated. Similarly, binding of [3H]-nitrendipine to the calcium channel is not influenced. It is suggested that amantadine may exert its positive inotropic effect by interaction with the potassium channel, causing a delay in outward current.

symmetrel drug interactions 2016-03-13

Short-term tinnitus develops shortly after the administration of a high dose of salicylate. Since salicylate selectively potentiates N-methyl- D-aspartate (NMDA) currents in spiral ganglion neurons, it may play a vital role in tinnitus by amplifying NMDA-mediated neurotransmission. The aim of this study was to determine whether systemic treatment with a NMDA channel blocker, memantine, could prevent salicylate-induced tinnitus in animals. Additional experiments were performed to evaluate the effect of memantine on the auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE) to test for changes in hearing function. Thirty-six rats were divided into 3 groups and treated daily for four consecutive days. One group (n = 12) was injected with salicylate (300 mg/kg/d, IP), the second (n = 12) was treated with memantine (5 mg/kg/d, IP) and the third group (n = 12) was injected with salicylate and memantine. All rats were tested for tinnitus and hearing loss at 2, 24, 48 and 72 h after the first drug administration and 24 h post treatment; tinnituslike behaviour was assessed with gap prepulse inhibition of acoustic startle (GPIAS), and hearing function was measured with DPOAE, ABR and noise burst prepulse inhibition of acoustic startle (NBPIAS). Rats in the salicylate group showed impaired GPIAS indicative of transient tinnitus-like behaviour near 16 kHz that recovered 24 h after the last salicylate treatment. Memantine did not cause a significant change in GPIAS. Combined injection of salicylate and memantine significantly attenuated GPIAS tinnitus-like behaviour at 48 hours after the first injection. None of the treatments induced permanent threshold shifts in the ABR and DPOAE, which recovered completely within one day post treatment. Animals treated with salicylate plus memantine showed results comparable to animals treated with salicylate alone, confirming that there is no effect of memantine on DPOAE which reflects OHC function. The present study confirms the role of cochlear NMDA receptors in the induction of salicylate-induced tinnitus.

symmetrel user reviews 2017-04-23

Single doses of amantadine hydrochloride and placebo were administered in a double-blind cross-over design on separate days to ten actively craving cocaine abusers in treatment. Pharmacological treatment did influence cocaine craving, but amantadine was less effective than placebo.

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Vaccination with the influenza A transmembrane protein M2 provides enhanced viral clearance and recovery from influenza A virus infection in mice. However, the high degree of hydrophobicity of the protein limits its purification for vaccine purposes. We have attempted to alter the structure of the M2 protein to allow high level recombinant expression in Escherichia coli, to reduce its hydrophobicity and improve protein solubility, thus improving its properties as a vaccine subunit candidate. Constructs investigated include deletion of the transmembrane domain of M2 (residues 26-43) and an extended deletion (residues 26-55). A full-length M2 protein was not pursued because of poor expression, even in the presence of amantadine. Expressed as glutathione S-transferase fusion proteins and used to vaccinate mice, either deletion construct was found to raise M2-specific serum antibodies and enhance viral clearance in mice challenged with homologous and heterologous influenza A viruses. Enzymatic cleavage from the GST fusion domain produces soluble protein giving similar results. The results demonstrate that large alterations of M2 protein structure can improve its isolation and purification characteristics without detracting from its immunogenic properties.

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We reviewed the charts of 11 subjects with DLB by McKeith Criteria that were prospectively evaluated and treated with memantine (with or without cholinesterase inhibitors (ChEIs)) for varying lengths of time.

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The NMDA receptor agonist quinolinic acid (9 mM) was infused i.c.v. via ALZET osmotic minipumps for 2 weeks. This treatment produced a persistent, short-term memory deficit in the T-maze. Autoradiography revealed a decrease in the density of choline uptake sites in the hippocampus. Parallel s.c. infusion by another minipump of the uncompetitive NMDA receptor antagonist memantine (1-amino-3,5-dimethyladamantane, 20 mg/kg per day) or (+)-5-methyl-10,11-dihydro-5H-dibenzocyclohepten-5,10-imine maleate ((+)-MK-801, 0.31 mg/kg day) prevented the learning deterioration induced by quinolinic acid. The treatment with memantine resulted in steady-state serum levels of 1.2 mu M which, based on in vitro data, should assure inhibition of NMDA receptors and are similar to levels seen in the serum of demented patients treated with this agent. In naive animals this treatment had no effect on either learning or on ex vivo induction of long-term potentiation, indicating that under chronic conditions it is possible to obtain neuroprotective effects with NMDA receptor antagonists without negative effects on memory processes. This contrasts to some acute insults (e.g. ischaemia) where high doses of NMDA receptor antagonists that produce side effects are required.

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To describe the clinical effects of amantadine and propranolol in an agitated pediatric patient with cognitive deficits, hyperactivity, and hypersexualism secondary to "shaken-baby syndrome."

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Response to triple therapy of interferon alfa, ribavirin, and amantadine was similar to standard therapy of interferon alfa and ribavirin. Our results suggest that amantadine has no role in the management of HCV.

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Transmissible spongiform encephalopathies are characterised by the transformation of the normal cellular prion protein (PrP(C)) into an abnormal isoform (PrP(TSE)). Previous studies have shown that N-methyl-D-aspartate (NMDA) receptor antagonists can inhibit glutathione depletion and neurotoxicity induced by PrP(TSE) and a toxic prion protein peptide, PrP106-126, in vitro. NMDA receptor activation is known to increase intracellular accumulation of Ca(2+), resulting in up-regulation of arachidonic acid (AA) metabolism. This can stimulate the lipoxygenase pathways that may generate a number of potentially neurotoxic metabolites. Because of the putative relationship between AA breakdown and PrP106-126 neurotoxicity, we investigated AA metabolism in primary cerebellar granule neuron cultures treated with PrP106-126. Our studies revealed that PrP106-126 exposure for 30 min significantly up-regulated AA release from cerebellar granule neurons. PrP106-126 neurotoxicity was mediated through the 5-lipoxygenase (5-LOX) pathway, as shown by abrogation of neuronal death with the 5-LOX inhibitors quinacrine, nordihydroguaiaretic acid, and caffeic acid. These inhibitors also prevented PrP106-126-induced caspase 3 activation and annexin V binding, indicating a central role for the 5-LOX pathway in PrP106-126-mediated proapoptosis. Interestingly, inhibitors of the 12-lipoxygenase pathway had no effect on PrP106-126 neurotoxicity or proapoptosis. These studies clearly demonstrate that AA metabolism through the 5-LOX pathway is an important early event in PrP106-126 neurotoxicity and consequently may have a critical role in PrP(TSE)-mediated cell loss in vivo. If this is so, therapeutic intervention with 5-LOX inhibitors may prove beneficial in the treatment of prion disorders.