The N-demethylated derivative of the antipsychotic agent LOXAPINE that works by blocking the reuptake of norepinephrine, serotonin, or both. It also blocks dopamine receptors.
Drugs that bind to but do not activate SEROTONIN 5-HT2 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT2 RECEPTOR AGONISTS. Included under this heading are antagonists for one or more specific 5-HT2 receptor subtypes.
A dull or sharp painful sensation associated with the outer or inner structures of the eyeball, having different causes.
Techniques for standardizing and expediting taxonomic identification or classification of organisms that are based on deciphering the sequence of one or a few regions of DNA known as the "DNA barcode".
An involuntary contraction of a muscle or group of muscles. Spasms may involve SKELETAL MUSCLE or SMOOTH MUSCLE.
Subjectively experienced sensations in the absence of an appropriate stimulus, but which are regarded by the individual as real. They may be of organic origin or associated with MENTAL DISORDERS.
Discharge of URINE, liquid waste processed by the KIDNEY, from the body.
A pathologic condition of acid accumulation or depletion of base in the body. The two main types are RESPIRATORY ACIDOSIS and metabolic acidosis, due to metabolic acid build up.
A reduction in brain oxygen supply due to ANOXEMIA (a reduced amount of oxygen being carried in the blood by HEMOGLOBIN), or to a restriction of the blood supply to the brain, or both. Severe hypoxia is referred to as anoxia, and is a relatively common cause of injury to the central nervous system. Prolonged brain anoxia may lead to BRAIN DEATH or a PERSISTENT VEGETATIVE STATE. Histologically, this condition is characterized by neuronal loss which is most prominent in the HIPPOCAMPUS; GLOBUS PALLIDUS; CEREBELLUM; and inferior olives.
A prolonged seizure or seizures repeated frequently enough to prevent recovery between episodes occurring over a period of 20-30 minutes. The most common subtype is generalized tonic-clonic status epilepticus, a potentially fatal condition associated with neuronal injury and respiratory and metabolic dysfunction. Nonconvulsive forms include petit mal status and complex partial status, which may manifest as behavioral disturbances. Simple partial status epilepticus consists of persistent motor, sensory, or autonomic seizures that do not impair cognition (see also EPILEPSIA PARTIALIS CONTINUA). Subclinical status epilepticus generally refers to seizures occurring in an unresponsive or comatose individual in the absence of overt signs of seizure activity. (From N Engl J Med 1998 Apr 2;338(14):970-6; Neurologia 1997 Dec;12 Suppl 6:25-30)
A method of hemostasis utilizing various agents such as Gelfoam, silastic, metal, glass, or plastic pellets, autologous clot, fat, and muscle as emboli. It has been used in the treatment of spinal cord and INTRACRANIAL ARTERIOVENOUS MALFORMATIONS, renal arteriovenous fistulas, gastrointestinal bleeding, epistaxis, hypersplenism, certain highly vascular tumors, traumatic rupture of blood vessels, and control of operative hemorrhage.
A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults.
An application that must be submitted to a regulatory agency (the FDA in the United States) before a drug can be studied in humans. This application includes results of previous experiments; how, where, and by whom the new studies will be conducted; the chemical structure of the compound; how it is thought to work in the body; any toxic effects found in animal studies; and how the compound is manufactured. (From the "New Medicines in Development" Series produced by the Pharmaceutical Manufacturers Association and published irregularly.)
Drugs whose drug name is not protected by a trademark. They may be manufactured by several companies.
Exclusive legal rights or privileges applied to inventions, plants, etc.
Process that is gone through in order for a drug to receive approval by a government regulatory agency. This includes any required pre-clinical or clinical testing, review, submission, and evaluation of the applications and test results, and post-marketing surveillance of the drug.
An agency of the PUBLIC HEALTH SERVICE concerned with the overall planning, promoting, and administering of programs pertaining to maintaining standards of quality of foods, drugs, therapeutic devices, etc.
Pain in the pelvic region of genital and non-genital origin and of organic or psychogenic etiology. Frequent causes of pain are distension or contraction of hollow viscera, rapid stretching of the capsule of a solid organ, chemical irritation, tissue ischemia, and neuritis secondary to inflammatory, neoplastic, or fibrotic processes in adjacent organs. (Kase, Weingold & Gershenson: Principles and Practice of Clinical Gynecology, 2d ed, pp479-508)
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
Depressive states usually of moderate intensity in contrast with major depression present in neurotic and psychotic disorders.
Conditions or pathological processes associated with pregnancy. They can occur during or after pregnancy, and range from minor discomforts to serious diseases that require medical interventions. They include diseases in pregnant females, and pregnancies in females with diseases.
Acute or chronic pain in the lumbar or sacral regions, which may be associated with musculo-ligamentous SPRAINS AND STRAINS; INTERVERTEBRAL DISK DISPLACEMENT; and other conditions.
Control of drug and narcotic use by international agreement, or by institutional systems for handling prescribed drugs. This includes regulations concerned with the manufacturing, dispensing, approval (DRUG APPROVAL), and marketing of drugs.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
A synthetic morphinan analgesic with narcotic antagonist action. It is used in the management of severe pain.
A component of the Executive Office of the President established by the Anti-Drug Abuse Act of 1988. The Office establishes policies, priorities, and objectives for national DRUG AND NARCOTIC CONTROL. The goals of the program are to reduce illicit drug use, manufacturing, and trafficking, drug-related crime and violence, and drug-related health consequences.
Laws concerned with manufacturing, dispensing, and marketing of drugs.
A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).

Repeated propofol anesthesia for a patient with a history of neuroleptic malignant syndrome. (1/14)

Neuroleptic malignant syndrome (NMS) is the most serious side effect produced by the administration of antipsychotic drugs. NMS shares many clinical similarities with malignant hyperthermia (MH), but the etiology of NMS and the relation between NMS and MH remain unknown. Anesthetic regimens for patients with NMS are not well established. We gave repeated anesthesia to a patient with a history of NMS undergoing electroconvulsive therapy for the treatment of depression. Propofol and vecuronium were used in twelve consecutive ECT sessions without complications. In this case report, we describe the safe and satisfactory repeated use of propofol in a patient with a history of NMS, and outline NMS and its questionable relation to MH.  (+info)

Differential effects of the tricyclic antidepressant amoxapine on glycine uptake mediated by the recombinant GLYT1 and GLYT2 glycine transporters. (2/14)

We examined the effects of nine different tricyclic antidepressant drugs on the glycine uptake mediated by the glycine transporter 1b (GLYT1b) and glycine transporter 2a (GLYT2a) stably expressed in human embryonic kidney 293 cells. Desipramine, imipramine, clomipramine, nomifensine and mianserin had no effect on the activity of the glycine transporters. Doxepin, amitriptyline and nortriptyline inhibited the two transporter subtypes to a similar extent. Amoxapine displayed a selective inhibition of GLYT2a behaving as a 10 fold more efficient inhibitor of this isoform than of GLYT1b. Kinetic analysis of the initial rates of glycine uptake by GLYT2a as a function of either glycine, chloride or sodium concentration, in the absence and presence of amoxapine indicated that amoxapine behaved as a competitive inhibitor of both glycine and chloride and a mixed-type inhibitor with respect to sodium. A kinetic model was developed which explains adequately these data, and gives information about the order of binding of sodium and chloride ions to GLYT2a. Our results may contribute to the development of the glycine transporter pharmacology. Additionally, the inhibition of the glycine uptake by GLYT2 is suggested to have some role in the sedative and psychomotor side effects of amoxapine. British Journal of Pharmacology (2000) 129, 200 - 206  (+info)

Transformation of amoxapine by Cunninghamella elegans. (3/14)

We examined Cunninghamella elegans to determine its ability to transform amoxapine, a tricyclic antidepressant belonging to the dibenzoxazepine class of drugs. Approximately 57% of the exogenous amoxapine was metabolized to three metabolites that were isolated by high-performance liquid chromatography and were identified by nuclear magnetic resonance and mass spectrometry as 7-hydroxyamoxapine (48%), N-formyl-7-hydroxyamoxapine (31%), and N-formylamoxapine (21%). 7-Hydroxyamoxapine, a mammalian metabolite with biological activity, now can be produced in milligram quantities for toxicological evaluation.  (+info)

Loxapine intoxication: case report and literature review. (4/14)

Loxapine is a dibenzoxazepine tricyclic compound used to treat schizophrenia in the United States since 1976. Metabolism includes demethylation to its primary metabolite, amoxapine. There are few documented reports of the disposition of loxapine in deaths due to overdose. This report discusses the overdose suicide of a 69-year-old white female found dead in her home by her husband. A prescription for loxapine (50-mg capsules) was found near the body. An autopsy was performed and heart blood, bile, vitreous humor, and gastric contents were submitted for toxicological analysis. The blood specimen was subjected to comprehensive testing that included volatile analysis by headspace gas chromatography (GC); acidic/neutral and basic drug screening by GC; benzodiazepine screening by high-performance liquid chromatography; opiate screening by modified immunoassay; and acetaminophen, salicylate, and ethchlorvynol screening by colorimetry. Loxapine and amoxapine were detected in the basic drug screen. No other drugs were detected in the case specimens. The respective concentrations of loxapine and amoxapine in each specimen were as follows: heart blood, 9.5 and 0.6 mg/L; bile, 28.8 and 4.7 mg/L; gastric, 278 mg/L and negative; and vitreous, 1.5 mg/L and negative. A review of the literature showed that the heart blood concentration of loxapine measured in this case was the highest reported to date. Based on the autopsy findings, patient history, and toxicology results, the cause of death was determined to be acute intoxication of loxapine and the manner, suicide.  (+info)

Generic prescribing of antidepressants. (5/14)

Analysis of National Health Service prescription data for the antidepressants from 1980 to 1989 shows a consistent secular trend towards the increased use of generic names on prescriptions for this group of drugs. This apparently reflects national trends for all drugs, and was similar for most antidepressants. However, generic prescribing had by 1989 increased significantly more rapidly with fluvoxamine, which was introduced in 1987. The two drugs introduced in 1989, fluoxetine and amoxapine, also had a high generic prescribing rate in their year of introduction. Increased generic prescribing may become a feature with further new drugs. However, the use of the generic name on the prescription has relatively little influence on what is dispensed to the patient. Pharmacists may dispense a brand name when given a generic prescription. Moreover, pressures on doctors to write generic names on prescriptions may have limited relevance for some drugs; generic alternatives were available for only four out of 22 antidepressants.  (+info)

Amoxapine as an atypical antipsychotic: a comparative study vs risperidone. (6/14)

Amoxapine is marketed as an antidepressant. However, its in-vitro profile, receptor occupancy and preclinical effects are very similar to atypical antipsychotics. Amoxapine has also shown efficacy as an atypical antipsychotic in open trials. The objective of this study was to compare the antipsychotic and side effect profile of amoxapine and risperidone in a randomised assignment, standardized dosing, double-blind trial of acutely psychotic patients with schizophrenia. A total of 48 schizophrenic patients were enrolled and randomized in a double-blind 6-week trial to receive either risperidone (up to 5 mg/day) or amoxapine (up to 250 mg/day). Positive, negative, affective symptoms and motor side effects were measured using standardized weekly assessments. Prolactin levels were also determined at baseline and at the end of the study. A total of 39 patients (amoxapine, n=22; risperidone, n=21) completed the trial. Both pharmacological treatments, amoxapine 228.0 mg/day (SD=34.6) and risperidone 4.5 mg/day (SD=0.7), showed equivalent improvement in positive, negative, and depressive symptoms. Amoxapine was associated with less EPS and less prolactin elevation than risperidone. These data support previous reports about the efficacy of amoxapine as an atypical antipsychotic. Since amoxapine is off-patent, it may be a valuable low-cost alternative to new atypical antipsychotics, particularly in low-income countries where the majority of the patients are still treated with typical antipsychotics.  (+info)

Amoxapine inhibits the delayed rectifier outward K+ current in mouse cortical neurons via cAMP/protein kinase A pathways. (7/14)

 (+info)

Inhibition of G protein-activated inwardly rectifying K+ channels by different classes of antidepressants. (8/14)

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To the editor: In the cases reported by Goldberg and Spector (1), the development of permanent neurologic deficits in two patients was attributed to the toxic effects of amoxapine. We question this conclusion, and feel that a more reasonable cause for the neurologic sequellae was cerebral anoxia or severe metabolic acidosis.. Both patients presented with coma, multiple seizures, and metabolic acidosis after large overdoses of amoxapine. The neurologic damage in these two patients may have had several responsible mechanisms. Central nervous system morbidity and mortality are not uncommon after status epilepticus and are felt to reflect the duration of the ...
TY - JOUR. T1 - Determination of D-alanine in the rat central nervous system and periphery using column-switching high-performance liquid chromatography. AU - Morikawa, Akiko. AU - Hamase, Kenji. AU - Zaitsu, Kiyoshi. PY - 2003/1/1. Y1 - 2003/1/1. N2 - A column-switching chiral HPLC system for the determination of minute amounts of D-Ala in mammalian tissues has been established. D-Ala and its L-enantiomer are purified as a DL mixture on a micro-ODS column after precolumn fluorescence derivatization with 4-fluoro-7-nitro-2,1,3-benzoxadiazole and are introduced to a chiral column to determine each enantiomer. The calibration curve of D-Ala spiked into a rat cerebellum sample is linear from 5 to 5000 fmol with a correlation coefficient of 1.0000. The lower limit of quantitation of D-Ala is 5 fmol (S/N = 5). Within-day and day-to-day precisions of spiked D-Ala (15 fmol) are 3.9 and 4.8% (R.S.D), respectively. With this system, the anatomical distribution of free D-Ala in the rat central nervous ...
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Drugs may be covered by multiple patents or regulatory protections. All trademarks and applicant names are the property of their respective owners or licensors. Although great care is taken in the proper and correct provision of this service, thinkBiotech LLC does not accept any responsibility for possible consequences of errors or omissions in the provided data. The data presented herein is for information purposes only. There is no warranty that the data contained herein is error free. thinkBiotech performs no independent verifification of facts as provided by public sources nor are attempts made to provide legal or investing advice. Any reliance on data provided herein is done solely at the discretion of the user. Users of this service are advised to seek professional advice and independent confirmation before considering acting on any of the provided information. thinkBiotech LLC reserves the right to amend, extend or withdraw any part or all of the offered service without notice. ...
The IUPHAR/BPS Guide to Pharmacology. amoxapine ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
Many women during their pregnancy experience different types of pain like pelvic pain, knee pain, back pain etc., which is due to the hormonal changes in their body and weight gain during pregnancy. Apart from pain, many women also face depression during their pregnancy or breastfeeding. In both phases of their lives, it becomes difficult to decide which medications they should consider to eradicate pain or manage depression. During pregnancy or breastfeeding a woman has to always think about her baby before taking any medication as they are not aware about how the medication is going to work for them or their baby.. While pregnancy is believed to be the period of joy, but this is not the case for every woman. At least one out of 10 pregnant women suffer from depression. Due to the fluctuation in hormones during pregnancy, many women face depression.. Same thing can happen in case of nursing mother who after the birth of their baby find it difficult to manage depression. In such situations both ...
Tell your doctor if your symptoms do not get better or if they get worse. Visit your doctor or health care professional for regular checks on your progress. Because it may take several weeks to see the full effects of this medicine, it is important to continue your treatment as prescribed by your doctor.. Patients and their families should watch out for new or worsening thoughts of suicide or depression. Also watch out for sudden changes in feelings such as feeling anxious, agitated, panicky, irritable, hostile, aggressive, impulsive, severely restless, overly excited and hyperactive, or not being able to sleep. If this happens, especially at the beginning of treatment or after a change in dose, call your health care professional.. You may get drowsy or dizzy. Do not drive, use machinery, or do anything that needs mental alertness until you know how this medicine affects you. Do not stand or sit up quickly, especially if you are an older patient. This reduces the risk of dizzy or fainting ...
Tell your doctor if your symptoms do not get better or if they get worse. Visit your doctor or health care professional for regular checks on your progress. Because it may take several weeks to see the full effects of this medicine, it is important to continue your treatment as prescribed by your doctor.. Patients and their families should watch out for new or worsening thoughts of suicide or depression. Also watch out for sudden changes in feelings such as feeling anxious, agitated, panicky, irritable, hostile, aggressive, impulsive, severely restless, overly excited and hyperactive, or not being able to sleep. If this happens, especially at the beginning of treatment or after a change in dose, call your health care professional.. You may get drowsy or dizzy. Do not drive, use machinery, or do anything that needs mental alertness until you know how this medicine affects you. Do not stand or sit up quickly, especially if you are an older patient. This reduces the risk of dizzy or fainting ...
Tell your doctor if your symptoms do not get better or if they get worse. Visit your doctor or health care professional for regular checks on your progress. Because it may take several weeks to see the full effects of this medicine, it is important to continue your treatment as prescribed by your doctor.. Patients and their families should watch out for new or worsening thoughts of suicide or depression. Also watch out for sudden changes in feelings such as feeling anxious, agitated, panicky, irritable, hostile, aggressive, impulsive, severely restless, overly excited and hyperactive, or not being able to sleep. If this happens, especially at the beginning of treatment or after a change in dose, call your health care professional.. You may get drowsy or dizzy. Do not drive, use machinery, or do anything that needs mental alertness until you know how this medicine affects you. Do not stand or sit up quickly, especially if you are an older patient. This reduces the risk of dizzy or fainting ...
Tell your doctor if your symptoms do not get better or if they get worse. Visit your doctor or health care professional for regular checks on your progress. Because it may take several weeks to see the full effects of this medicine, it is important to continue your treatment as prescribed by your doctor.. Patients and their families should watch out for new or worsening thoughts of suicide or depression. Also watch out for sudden changes in feelings such as feeling anxious, agitated, panicky, irritable, hostile, aggressive, impulsive, severely restless, overly excited and hyperactive, or not being able to sleep. If this happens, especially at the beginning of treatment or after a change in dose, call your health care professional.. You may get drowsy or dizzy. Do not drive, use machinery, or do anything that needs mental alertness until you know how this medicine affects you. Do not stand or sit up quickly, especially if you are an older patient. This reduces the risk of dizzy or fainting ...
Confusion; sexual dysfunction; heartbeat irregularities; hallucinations; seizures; extreme fatigue or drowsiness; blurred or altered vision; breathing difficulty; constipation; staring and absence of facial expression; impaired concentration; difficult urination; fever; extreme and persistent restlessness; loss of coordination and balance; difficulty swallowing or speaking; dilated pupils; eye pain; fainting; trembling, shaking, weakness, and stiffness in the extremities; shuffling gait; persistent, uncontrolled chewing, lip-smacking, or tongue movements; uncontrolled movements, including tics, twitching, twisting movements, and muscle spasms in the face, arms hands, and legs. Call your doctor immediately ...
Selective Serotonin Reuptake Inhibitors The seven available agents in the selective serotonin reuptake inhibitor class are citalopram (Lund-becks Cipramil, Forest Laboratories Celexa, generics) and its single enan-tiomer, escitalopram (Lundbecks Cipralex, Forests Lexapro); paroxetine (GSKs Paxil/Seroxat, Novartiss Frosinor, generics); the controlled-release version of paroxetine (GSKs Paxil CR); sertraline (Pfizers Zoloft); fluoxetine (Eli Lillys Prozac, generics); and… Read More ». ...
Examples include: drugs prescription without prednisone a Mood-congruent phenomenon of childbirth. Sexual dysfunction: Overview sexual assault: Management principles other issues regarding compliance identied for stress varies widely between countries and that the pharmacist collects and documents relevant information recorded from hypertensive disease and I serum -ht; some have an organic cause. X x x pm total fig. Tam, y. K. Immunostimulatory oligonucleotides: Ready for immuno- therapy prime time. In the uk, as it is not specic. Distribution of uid replacement alone will result in any format, such as amoxapine a tetracyclic antidepressant with the patient, and clearly marked with an average of two variables may be normal. Could be used, in particular chronic headache. Ensure patient is already on antipsychotic then consider pulmonary embolus consider empirical anticoagulation early and check for sensory loss in an kg adult over a joint after clinical examination indicate the use of technology ...
Aura-Soma è un sistema olistico non intrusivo, concepito nel da Vicky Wall, erborista e farmacista inglese, che amalgama armonicamente qualità dei colori, delle essenze aromatiche e le vibrazioni dei cristalli.‎Punti vendita · ‎Corsi · ‎Filosofia · ‎Libri. With over 30 years experience Aura-Soma is a non-intrusive, self-selective soul system. Combining the energies of colour, plants, and crystals, these vibrational tools can support all levels of our being, bringing harmony and balance within the subtle fields promoting wellbeing and a joy for life. Such antidepressants double amitriptyline (Elavil, Endep), desipramine (Norpramin), doxepin (Sinequan), imipramine (Tofranil), amoxapine (Asendin), nortriptyline (Pamelor, Aventyl), and maprotiline (Ludiomil). Its dried aura soma italy pain, aura soma italy down pain from my little lower back all the way to the hair ankle. Disagreeable I sit down it has but I literally cant recall for more than about interactions at a time,the pain ...
Do not take Generic Eldepryl if you are allergic to Generic Eldepryl components.. Do not take Generic Eldepryl if you are pregnant, planning to become pregnant or breast-feeding.. Be careful using Generic Eldepryl if you have kidney disease, liver disease, heart disease, high or low blood pressure, seizure disorder.. Be careful using Generic Eldepryl if you take over-the-counter medications you use, including vitamins, minerals, and herbal products, carbamazepine (Tegretol), diet pills or cold medicines that contain ephedrine, pseudoephedrine or phenylephrine, nafcillin (Unipen), phenobarbital (Luminal, Solfoton), rifampin (Rifadin, Rifater, Rifamate, Rimactane), antidepressants such as amitriptyline (Elavil), amoxapine (Ascendin), bupropion (Wellbutrin, Zyban), citalopram (Celexa), clomipramine (Anafranil), desipramine (Norpramin), doxepin (Sinequan), duloxetine (Cymbalta), escitalopram (Lexapro), fluoxetine (Prozac), fluvoxamine (Luvox), imipramine (Tofranil), nortriptyline (Pamelor), ...
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Abilify, Adapin, Adderall, Alepam, Alertec, Aloperidin, Alplax, Alprax, Alprazolam, Alviz, Alzolam, Amantadine, Ambien, Amisulpride, Amitriptyline, Amoxapine, Anafranil, Anatensol, Ansial, Ansiced, Antabus, Antabuse, Antideprin, Anxiron, Apo-Alpraz, Apo-Primidone, Apo-Sertral, Aponal, Apozepam, Aripiprazole, Aropax, Artane, Asendin, Asendis, Asentra, Ativan, Atomoxetine, Aurorix, Aventyl, Axoren. ...
The aim of this study was to explore associated factors of post-stroke depression (PSD) among Chinese first-time stroke patients. A 6-month prospective design was adopted with data collected by face-to-face interviews and physical assessment at two observation time points: T1, within 48 h of admission to the rehabilitation hospitals and T2, 6 months after the first interview in the subjects current place of residence. The prevalence of PSD at T1 and T2 was found to be 69% and 48% respectively. Backward linear regression showed that five variables explained 55% of the variance of PSD at T2. Participants who had a higher level of depression at T2 tended to have a higher level of functional disability, less social companionship and poorer informational support. Those who had been homemaker at pre-morbid state and those who exhibited a higher level of depressive symptoms at T1 showed a higher level of depression at T2. The results of this study suggest that PSD could be a psychological condition ...
Objectives People who suffer a stroke are at risk of developing post-stroke depression (PSD). Not only does this lower their quality of life but it also increases their risk of another stroke or death. This study aimed to investigate the factors associated with PSD in order to better direct rehabilitation efforts aimed at cutting the incidence of PSD.. Material and methods This study was based on all patients admitted to the stroke unit of a hospital in southern Sweden from 1 October 2003 to 30 November 2005. The total number of patients involved was 181. Measures were collected at 2 +/- 1 weeks after discharge from hospital, 3 +/- 0.5 months after the occurrence of the stroke and 12 +/- 1 months after the occurrence of the stroke. Information collected was results from the Center of Epidemiologic Studies Depression Scale and the Barthel Index together with demographic data including age, sex, time since stroke and relationship status.. Results Those patients involved in the study were mainly ...
Drug interactions can alter the way you work with medications or increase the risk of serious side effects. This document does not cover all possible drug interactions. Keep a list of all the products you use (including medicines, prescription / non-prescription, and herbal products) and tell them to your doctor and pharmacist. Do not start, stop or change the dose of a drug without the doctors permission.. Some products that may interact with this drug include: anticholinergics (eg, atropine, alkaloid bell), some antihypertensive medicines (eg, clonidine, guanethidine, reserpine), travel sickness medication (eg, meclizine), psychotropic drugs (for example, antipsychotics, antidepressants ), Thyroid preparations.. ...
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A variety of emotional and behavioural disorders may develop following stroke. In stroke, prevalence rates of depression and anxiety have been reported to be as high as 24% and 29% respectively. These rates may be influenced by a combination of factors such as age, sex, socioeconomic factors, functional independence post-stroke, and the presence of cognitive disorders post-stroke which play a crucial role in an individuals emotional well-being and can significantly impact recovery. Many studies have investigated pharmacological and non-pharmacological treatment options for post-stroke mood disturbances; however, no consensus has been reached regarding the most effective and viable treatment option available although the most effective treatment option appears to be pharmacological. This chapter explores the evidence of the various interventions on reducing post-stroke depression and other mood disorders, and delves into the possible risk factors that can facilitate the occurrence of post-stroke ...
This trial will compare outcomes in depressed patients receiving the Activate-Initiate-Monitor (AIM) intervention vs. those receiving usual care, and will also compare outcomes in depressed and non-depressed stroke survivors. Patients are screened for depression 1 to 2 months post-stroke. Patients with depression are then randomized to the AIM intervention or control group. Patients without depression are also enrolled at the same time and are matched by hospital site to the depressed patients.. The AIM intervention is a 3-part program consisting of activating or educating the patient and his/her family about post-stroke depression, instituting treatment for depression, and monitoring antidepressant treatments for side effects, efficacy, and compliance. Control patients are evaluated and treated with usual care by their physicians. Patients without depression do not receive the intervention but complete the same assessments on the same schedule as the patients with depression. ...
Stroke patients who are not successfully treated for depression are at higher risk of losing some of their capability to function normally, according to a study in the March 15, 2011 issue of the journal Neurology.. Although as many as a third of those who experience a stroke develop depression, a new study by researchers from the Regenstrief Institute, the schools of health and rehabilitation sciences and of medicine at Indiana University-Purdue University Indianapolis and the Richard L. Roudebush VA Medical Center is the first to look whether managing post-stroke depression improves physical functioning.. They researchers report that individuals who remain depressed three months after a stroke are more likely to have decreased functional capabilities than those whose depression was successfully treated. Functional capabilities include getting dressed, feeding oneself, and accomplishing other tasks. These capabilities increased significantly in those individuals who were treated for ...
Translational Psychiatry, Published online: 30 September 2020; doi:10.1038/s41398-020-01008-9Fluoxetine-induced recovery of serotonin and norepinephrine projections in a mouse model of post-stroke depression...
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This study presents the development and performance of a clinical prediction model with its accompanying risk-assessment table to identify admitted stroke patients able to communicate adequately, who are at increased risk for PSD. The DePreS showed acceptable discrimination and calibration.. The structural use of a screening instrument in the daily care of stroke patients will promote the early recognition of depression.5,23 The trend toward decreasing hospital stays6 complicates proper screening for PSD during hospital stay4 and emphasizes the need for an easy-to-use prediction model to identify the risk for PSD. Our aim was to develop a prediction model that clinicians can apply in the daily care during the first week after stroke. Although a systematic review showed that several studies have been conducted on the prediction of PSD, the overall conclusion was that most of the available models lack precision, were not thoroughly developed or validated and were not clinically useful.11 In this ...
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Pro-Mirtazapine: Mirtazapine belongs to the group of medications known as tetracyclic antidepressants. Antidepressants are used to help relieve the symptoms of depression such as feeling low, sleeping problems, loss of appetite, and loss of interest in activities that you would normally enjoy doing.
This is an in-clinic, multi-center, randomized, double-blind, placebo-controlled study of 2 dose levels of Staccato Loxapine, 5 and 10 mg. Patients may receive up to 3 doses of study drug in a 24-hour period, depending on their clinical status. The primary endpoint is the change from baseline in the PANSS (Positive and Negative Symptom Scale) Excited Component (also known as PEC) score, performed at 2 hours after the first dose ...
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tell your doctor and pharmacist what prescription and nonprescription medications, vitamins, and nutritional supplements you are taking or plan to take. Be sure to mention any of the following: anticoagulants (blood thinners) such as warfarin (Coumadin, Jantoven); antidepressants such as amitriptyline (Elavil), amoxapine (Asendin), clomipramine (Anafranil), desipramine (Norpramin), doxepin, imipramine (Tofranil), nortriptyline (Aventyl, Pamelor), protriptyline (Vivactil), and trimipramine (Surmontil); certain antifungals such as ketoconazole (Nizoral); buspirone; carbamazepine (Carbatrol, Epitol, Equetro, Tegretol, other); cimetidine (Tagamet); diazepam (Valium); erythromycin (E.E.S., E-mycin, Erythrocin); fentanyl (Abstral, Actiq, Fentora, Onsolis, others); lithium (Eskalith, Lithobid); medications for migraine headaches such as almotriptan (Axert), eletriptan (Relpax), frovatriptan (Frova), naratriptan (Amerge), rizatriptan (Maxalt), sumatriptan (Imitrex), and zolmitriptan (Zomig); certain ...
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Definition of maprotiline in US English - A tetracyclic antidepressant with properties similar to those of tricyclic amitriptyline, usually administered orally as
Abstract: The tetracyclic antidepressant mirtazapine has been in clinical use for several years as a racemic drug. Because of a… Expand ...
Trazodone is a tetracyclic antidepressant. It is thought to increase the activity of one of the brain chemicals (serotonin), which helps elevate mood. The active ingredient in Desyrel®, T...
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Results of the research appear the week of What this study shows more convincingly than in the past is that the production of new involve screening any of the existing drugs neurons after stroke is beneficial in rodents, that support neurogenesis, compared stroke said Buck faculty member. Assuming that neurogenesis is also beneficial in humans, genetically altered and treated to either grow or not grow new neurons prior to stroke. purposes and already shown to promote new percent larger in the animals that did not studying as a potential treatment for stroke grow new neurons; the rodents that did grow in humans. For example, antidepressants are often used to treat post-stroke depression, in motor function following the stroke. The but their potential for improving outcome exact mechanism by which the new neurons Previous research by the same group at the Although the possibility of using existing drugs for the treatment of stroke is one that attempts to heal itself following stroke by may ...
We use experimental models to understand the short-term and long term consequences of ischemic stroke, and our goal is to develop stroke therapies, using compounds that can modify the brain and immune system, to improve stroke recovery.. We are especially interested in sex differences in stroke. Young females are less likely to experience a stroke as compared to young males. However, after the age of 50+, women are equally likely to suffer a stroke as compared to men. At older ages, many more women will get a stroke as compared to men, and their stroke are likely to be worse, resulting in greater mortality, disability and loss of independence. Women are also more likely to exhibit post-stroke depression.. Stroke outcomes can be modified by environmental and developmental factors, and in turn stroke can also lead to other disabilities, such as epilepsy, addiction, depression. In conjunction with our colleagues at the TAMHSC COM and TAMIN, we are studying these issues in an animal model.. Stroke ...
Introduction: Post-Stroke Depression (PSD) is one of the stroke complications characterized by mood abnormality, self-blame, and grief diagnosed in 40-72% of stroke patients. PSD is a major factor that can inhibit the ...
Throughout my career, I have examined the utility of existing neuropsychological tests to detect, quantify, and differentially diagnose neurodegenerative diseases and other neurological conditions. However, when there were inadequate existing measures to answer clinical and research needs, I developed and published a new instrument. For example, in my early studies of post-stroke depression, there was a need for an instrument to measure various mood states in patients with aphasia and cognitive impairment. I, therefore, developed the Visual Analog Mood Scales (VAMS). In addition, based upon my training in the Process Approach to neuropsychological assessment under Dr. Edith Kaplan, I developed the Boston Qualitative Scoring System (BQSS) for the Rey-Osterreith Complex Figure (ROCF) with colleagues and trainees, thus creating a more comprehensive and sensitive method of evaluating and quantifying the rich information previously missed in previous methods of scoring the commonly used ROCF. And, ...
AMOXAPINE 8. AZACICLONOL 9. BECLAMIDE 10. BENACTIZIN 11. BENFLUOREX 12. BENZOCTAMINE 13. BENZOQUINAMIDE 14. BIPERIDENE 15. ...
Amoxapine • Buspirone • Butaclamol • Ecopipam • N-Ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) • Eticlopride • ...
... is an active metabolite of amoxapine (Asendin). It contributes to amoxapine's pharmacology. Amoxapine Jue, ... Calvo, B; García, MJ; Pedraz, JL; Mariño, EL; Domínguez-Gil, A (April 1985). "Pharmacokinetics of amoxapine and its active ... SG; Dawson, GW; Brogden, RN (July 1982). "Amoxapine: A Review of its Pharmacology and Efficacy in Depressed States". Drugs. 24 ...
Amoxapine, etc.) Antihistamines (Cyproheptadine, Hydroxyzine, Latrepirdine, etc.) Antipsychotics Typicals (Chlorpromazine, ...
Tetracyclic antidepressants (TeCAs): amoxapine, maprotiline. Phenylpiperidine derivative opioids: meperidine/pethidine, ...
... causes arterial/arteriolar vasodilation leading to a decrease in blood pressure by activating peripheral D1 receptors.[5] It decreases afterload and also promotes sodium excretion via specific dopamine receptors along the nephron. The renal effect of fenoldopam and dopamine may involve physiological antagonism of the renin-angiotensin system in the kidney.[6] In contrast to dopamine, fenoldopam is a selective D1 receptor agonist with no effect on beta adrenoceptors, although there is evidence that it may have some alpha-1 [7] and alpha-2 adrenoceptor antagonist activity.[5] D1 receptor stimulation activates adenylyl cyclase and raises intracellular cyclic AMP, resulting in vasodilation of most arterial beds, including renal, mesenteric, and coronary arteries.[8] to cause a reduction in systemic vascular resistance. Fenoldopam has a rapid onset of action (4 minutes) and short duration of action (, 10 minutes) and a linear dose-response relationship at usual clinical doses.[9] ...
Tetracyclic antidepressants (e.g., amoxapine, loxapine, maprotiline, mianserin, mirtazapine, oxaprotiline). *Tricyclic ... Tetracyclic antidepressants (e.g., amoxapine, aptazapine, esmirtazapine, maprotiline, mianserin, mirtazapine). *Tricyclic ... Tetracyclic antidepressants (e.g., amoxapine, mianserin). *Tricyclic antidepressants (e.g., amitriptyline, clomipramine, ... Tetracyclic antidepressants (e.g., amoxapine, maprotiline, mianserin, mirtazapine). *Tricyclic antidepressants (e.g., ...
The hormone prolactin stimulates lactation (production of breast milk). Dopamine, released by the hypothalamus stops the release of prolactin from the pituitary gland. Domperidone, by acting as an anti-dopaminergic agent, results in increased prolactin secretion, and thus promotes lactation (that is, it is a galactogogue). In some nations, including Australia, domperidone is used off-label, based on uncertain and anecdotal evidence of its usefulness, as a therapy for mothers who are having difficulty breastfeeding.[24][25] In the United States, domperidone is not approved for this or any other use.[26][27] A study called the EMPOWER trial was designed to assess the effectiveness and safety of domperidone in assisting mothers of preterm babies to supply breast milk for their infants.[28] The study randomized 90 mothers of preterm babies to receive either domperidone 10 mg orally three times daily for 28 days (Group A) or placebo 10 mg orally three times daily for 14 days followed by domperidone ...
Amoxapine. *Antihistamines (e.g., brompheniramine, chlorphenamine, dimenhydrinate, diphenhydramine, mepyramine (pyrilamine), ...
Tetracyclic antidepressants (e.g., amoxapine, aptazapine, esmirtazapine, maprotiline, mianserin, mirtazapine). *Tricyclic ... Tetracyclic antidepressants (e.g., amoxapine, mianserin). *Tricyclic antidepressants (e.g., amitriptyline, clomipramine, ... Tetracyclic antidepressants (e.g., amoxapine, maprotiline, mianserin, mirtazapine). *Tricyclic antidepressants (e.g., ...
Amoxapine. *Antihistamines (e.g., brompheniramine, chlorphenamine, dimenhydrinate, diphenhydramine, mepyramine (pyrilamine), ...
Amoxapine. *Antihistamines (e.g., brompheniramine, chlorphenamine, dimenhydrinate, diphenhydramine, mepyramine (pyrilamine), ...
Djaldetti Ruth; Giladi Nir; Hassin-Baer Sharon; Shabtai Hertzel; Melamed Eldad (November-December 2003). "Pharmacokinetics of Etilevodopa Compared to Levodopa in Patient's With Parkinson's Disease: An Open-label, Randomized, Crossover Study". Clinical Neuropharmacology. 26 (6): 322-326. doi:10.1097/00002826-200311000-00012. PMID 14646613 ...
Tetracyclic antidepressants (e.g., amoxapine, aptazapine, esmirtazapine, maprotiline, mianserin, mirtazapine). *Tricyclic ... Tetracyclic antidepressants (e.g., amoxapine, mianserin). *Tricyclic antidepressants (e.g., amitriptyline, clomipramine, ... Tetracyclic antidepressants (e.g., amoxapine, maprotiline, mianserin, mirtazapine). *Tricyclic antidepressants (e.g., ...
Amoxapine. *Antihistamines (e.g., brompheniramine, chlorphenamine, dimenhydrinate, diphenhydramine, mepyramine (pyrilamine), ... Tetracyclic antidepressants (e.g., amoxapine, maprotiline, mianserin). *Tricyclic antidepressants (e.g., amitriptyline, ... Tetracyclic antidepressants (e.g., amoxapine, aptazapine, esmirtazapine, maprotiline, mianserin, mirtazapine). *Tricyclic ... Tetracyclic antidepressants (e.g., amoxapine, mianserin). *Tricyclic antidepressants (e.g., amitriptyline, clomipramine, ...
Amoxapine. *Antihistamines (e.g., brompheniramine, chlorphenamine, dimenhydrinate, diphenhydramine, mepyramine (pyrilamine), ...
Melis MR, Succu S, Sanna F, Melis T, Mascia MS, Enguehard-Gueiffier C, Hubner H, Gmeiner P, Gueiffier A, Argiolas A (October 2006). "PIP3EA and PD-168077, two selective dopamine D4 receptor agonists, induce penile erection in male rats: site and mechanism of action in the brain". The European Journal of Neuroscience. 24 (7): 2021-30. doi:10.1111/j.1460-9568.2006.05043.x. PMID 17067298 ...
The present meta-analysis was conducted to estimate the magnitude of the effects of methylphenidate and amphetamine on cognitive functions central to academic and occupational functioning, including inhibitory control, working memory, short-term episodic memory, and delayed episodic memory. In addition, we examined the evidence for publication bias. Forty-eight studies (total of 1,409 participants) were included in the analyses. We found evidence for small but significant stimulant enhancement effects on inhibitory control and short-term episodic memory. Small effects on working memory reached significance, based on one of our two analytical approaches. Effects on delayed episodic memory were medium in size. However, because the effects on long-term and working memory were qualified by evidence for publication bias, we conclude that the effect of amphetamine and methylphenidate on the examined facets of healthy cognition is probably modest overall. In some situations, a small advantage may be ...
Tetracyclic antidepressants (e.g., amoxapine, maprotiline, mianserin). *Tricyclic antidepressants (e.g., amitriptyline, ...
... is a synthetic compound that acts as a selective antagonist on D2 dopamine receptors.[1] Its selectivity to the cerebral D2 receptors is characterized by its respective Ki-values, which are as follows: 1.8, 3.5, 2400 and 18000 nM for D2, D3, D4 and D1 receptors respectively. It can be radiolabelled with radioisotopes, e.g. 3H or 11C and used as a tracer for in vitro imaging (autoradiography) as well as in vivo imaging positron emission tomography (PET). Images obtained by cerebral PET scanning (e.g. PET/CT or PET/MRI) allow the non-invasive assessment of the binding capacity of the cerebral D2 dopamine receptor, which can be useful for the diagnosis of movement disorders. In particular, cerebral D2 receptor binding as measured by carbon-11-raclopride (11C-raclopride) has shown to reflect disease severity of Huntington's disease, a genetical disease characterized by selective degeneration of cerebral D2 receptors.[2] Other studies have investigated the relationship of D2 receptor ...
In 1960 the Austrian biochemist Oleh Hornykiewicz, while at the University of Vienna, examined results of autopsies of patients who had died with Parkinson's disease. He suggested that the disease was associated with, or caused by, a reduction in the levels of dopamine in the basal ganglia of the brain. Since dopamine itself did not enter the brain, he tried treating twenty patients with a racemic mixture of dihydroxyphenylalanine (DOPA), which could enter the brain and be converted there to dopamine by the action of DOPA decarboxylase. His results were positive, as were those of another trial in Montreal run by André Barbeau. Unfortunately, other investigators were unable to replicate these early results, and the use of DOPA remained in question until 1967, when George Cotzias at the Brookhaven National Laboratories in Upton, New York, used megadoses of DOPA, up to 16 grams per day. Not long after these results became known, Curt Porter at Merck showed that L-DOPA was the active stereoisomer, ...
InChI=1S/C20H33N3O3S/c1-4-10-22-14-17(21-27(25,26)23(5-2)6-3)11-16-12-18-15(13-19(16)22)8-7-9-20(18)24/h7-9,16-17,19,21,24H,4-6,10-14H2,1-3H3/t16-,17+,19-/m1/s1 ...
Joanna D. Moody; Donglu Zhang; Thomas M. Heinze; Carl E. Cerniglia (2000). "Transformation of amoxapine by Cunninghamella ...
Joanna D. Moody; Donglu Zhang; Thomas M. Heinze; Carl E. Cerniglia (2000). "Transformation of amoxapine by Cunninghamella ...
Nortriptyline, desipramine, and amoxapine are tricyclic antidepressants and secondary amines. (The tricyclics are grouped by ...
... is metabolized to amoxapine, as well as its 8-hydroxy metabolite (8-hydroxyloxapine). Amoxapine is further metabolized ... Amoxapine Clotiapine Truven Health Analytics, Inc. DrugPoint® System (Internet) [cited 2013 Sep 21]. Greenwood Village, CO: ... Loxapine may be metabolized by N-demethylation to amoxapine, a tricyclic antidepressant. The US Food and Drug Administration ( ... Cheung SW, Tang SW, Remington G (March 1991). "Simultaneous quantitation of loxapine, amoxapine and their 7- and 8-hydroxy ...
Some weak and/or non-selective GlyT blockers include amoxapine and ethanol (alcohol). Reuptake inhibitor Glycinergic GABA ...
Kurland published 14 articles on antidepressant medications, including nialamide, aletamine, dilantin, amoxapine among others. ...
With the exception of amoxapine, TeCAs do not inhibit the reuptake of serotonin[citation needed]. However, aside from ... Amoxapine (Asendin) - often classified as a TCA and grouped with the secondary amines Benzoctamine (Tacitin) - a tetracyclic ... a typical antipsychotic that produces amoxapine as a major metabolite and is said to have antidepressant effects, but it is not ...
Amoxapine does not have the TCA side chain and hence is neither a tertiary nor secondary amine, although it is often grouped ... amoxapine). In addition to classification based on the ring system, TCAs can also be usefully grouped based on the number of ... Amoxapine (Asendin) - can be classed with the TeCAs but more frequently classed with the TCAs Demexiptiline† (Deparon, Tinoran ...
Amoxapine first received marketing approval in the United States in 1992 (approximately 30 to 40 years after most of the other ... Amoxapine, sold under the brand name Asendin among others, is a tetracyclic antidepressant (TeCA). It is the N-demethylated ... In excess of 80% of patients that do respond to amoxapine are reported to respond within two weeks of the beginning of ... Its use is also advised against in individuals with known hypersensitivities to either amoxapine or other ingredients in its ...
Amoxapine: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Amoxapine comes as a tablet to take by mouth. It is usually taken one or more times a day. If you take amoxapine once a day, ... Continue to take amoxapine even if you feel well. Do not stop taking amoxapine without talking to your doctor. Your doctor ... Before taking amoxapine,. *tell your doctor and pharmacist if you are allergic to amoxapine, doxepin (Sinequan), any other ...
Home › Q & A › Questions › Please help! Amoxapine..... Please help! Amoxapine. Anyone take this med?. Asked. 22 May 2013 by ... Amoxapine is a wonderful drug. I have taken it since I was 24 and am now 63!! As I have chronic depression. I too had bad side ... Side Effects of Amoxapine (detailed). Search for questions. Still looking for answers? Try searching for what you seek or ask ... depression, anxiety, panic disorder, generalized anxiety disorder, amoxapine, side effect. Details:. My doctor wants me to try ...
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Amoxapine passes into breast milk; do not use it while nursing. Infants and Children. Not prescribed for children under the age ... Amoxapine affects levels of norepinephrine, a brain chemical that is thought to be linked to mood, emotions, and mental state. ...
Amoxapine tablets. What is this medicine?. AMOXAPINE (a MOX a peen) is used to treat depression. ... an unusual or allergic reaction to amoxapine, other medicines, foods, dyes, or preservatives ...
Amoxapine and Neurologic Deficits KEN KULIG, M.D.; BARRY H. RUMACK, M.D.; JOHN A. MARX, M.D. ... Amoxapine and Neurologic Deficits. Ann Intern Med. 1982;97:286. doi: 10.7326/0003-4819-97-2-286_2 ... Both patients presented with coma, multiple seizures, and metabolic acidosis after large overdoses of amoxapine. The neurologic ... the development of permanent neurologic deficits in two patients was attributed to the toxic effects of amoxapine. We question ...
Amoxapine testing. Laboratory testing for CAS number 14028-44-5. Dibenz[b,f][1,4]oxazepine, 2-chloro-11-(1-piperazinyl)-; ... Learn more about why Amoxapine is on the proposition 65 list (PDF). Date Listed: 15-May-98. Chemical Formula: C17H16ClN3O. ... Chemical Name: Amoxapine. Type of Toxicity: developmental Listing Mechanism: Formally Required to be labeled or identified (FR) ... 14028-44-5 Amoxapine. The Proposition 65 Chemical List information is provided for reference only and is subject to change. ...
Kudo K, Inoue H, Ishida T, Tsuji A, Ikeda N.A fatal case of amoxapine poisoning under the influence of chronic use of ... Amoxapine overdose. Death in a patient with chronic heart failure: case report ...
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Additional details are available on the AMOXAPINE profile page. The generic ingredient in AMOXAPINE is amoxapine. There are ... NDA 072879 describes AMOXAPINE, which is a drug marketed by Upsher-smith Labs, Watson Labs, and Watson Pharms Teva, and is ...
Eubacterium eligens beta-glucuronidase bound to an amoxapine-glucuronide conjugate. *DOI: 10.2210/pdb6D4O/pdb ...
... What is this medicine?. AMOXAPINE (a MOX a peen) is used to treat depression. ... an unusual or allergic reaction to amoxapine, other medicines, foods, dyes, or preservatives ...
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Category: Amoxapine. Learning about Amoxapine dosage and directions. Effective Amoxapine dosage can vary from one person to ... Amoxapine addiction is reported by a few so avoid taking Amoxapine in high doses. Amoxapine can lead to blurred vision; light ... Amoxapine drug interactions that can lead to complications. Some medicines can interact with Amoxapine. Let your health care ... Do not stop Amoxapine even if you start feeling better. It can take several weeks to get the maximum benefit of Amoxapine. ...
The N-demethylated derivative of the antipsychotic agent LOXAPINE that works by blocking the reuptake of norepinephrine, serotonin, or both. It also blocks dopamine receptors ...
AMOXAPINE 8. AZACICLONOL 9. BECLAMIDE 10. BENACTIZIN 11. BENFLUOREX 12. BENZOCTAMINE 13. BENZOQUINAMIDE 14. BIPERIDENE 15. ...

No data available that match "amoxapine"


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  • A small number of children, teenagers, and young adults (up to 24 years of age) who took antidepressants ('mood elevators') such as amoxapine during clinical studies became suicidal (thinking about harming or killing oneself or planning or trying to do so). (medlineplus.gov)
  • You should know that your mental health may change in unexpected ways when you take amoxapine or other antidepressants even if you are an adult over age 24. (medlineplus.gov)
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  • tell your doctor and pharmacist if you are allergic to amoxapine, doxepin (Sinequan), any other medications, or any of the inactive ingredients in amoxapine tablets. (medlineplus.gov)
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  • Amoxapine, sold under the brand name Asendin among others, is a tetracyclic antidepressant (TeCA). (wikipedia.org)
  • Amoxapine (amoxapine (amoxapine tablets) tablets) is an antidepressant of the dibenzoxazepine class, chemically distinct from the dibenzazepines, dibenzocycloheptenes, and dibenzoxepines. (rx-index.ru)
  • Amoxapine (brand-names Asendin ®, Asendis ®, Defanyl ®, Demolox ®, Moxadil ®) is a tetracyclic antidepressant of the dibenzoxazepine class. (wikia.org)
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  • The doctor or pharmacist will give you the manufacturer's patient information sheet (Medication Guide) when you begin treatment with amoxapine. (medlineplus.gov)
  • Amoxapine affects levels of norepinephrine, a brain chemical that is thought to be linked to mood, emotions, and mental state. (wholehealthmd.com)
  • Amoxapine is a strong reuptake inhibitor of norepinephrine and weak reuptake inhibitor of serotonin . (wikia.org)
  • Kudo K, Inoue H, Ishida T, Tsuji A, Ikeda N.A fatal case of amoxapine poisoning under the influence of chronic use of psychotropic drugs. (springer.com)
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  • Suggested maintenance Amoxapine dosage is the lowest possible dose that can maintain remission. (dealpain.net)
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  • Amoxapine (amoxapine (amoxapine tablets) tablets) is supplied for oral administration as 25 mg, 50 mg, 100 mg and 150 mg tablets. (rx-index.ru)
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  • Amoxapine can be prescribed as a single dose of not more than 300 mg to be taken daily ideally at bedtime. (dealpain.net)
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  • However, elderly patients are more likely to have unwanted effects (e.g., movement disorders, unusual drowsiness) or age-related kidney or liver problems, which may require an adjustment in the dose for patients receiving amoxapine. (pharmacypedia.org)
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  • Amoxapine first received marketing approval in the United States in 1992 (approximately 30 to 40 years after most of the other TCAs were introduced in the United States). (wikipedia.org)
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  • Because amoxapine has some effects that are similar to those of major tranquilizers , it may work better in patients who have agitation or anxiety along with depression . (webmd.com)
  • Because amoxapine has an effect similar to the effect of large sedatives, it can improve in patients who have anxiety or anxiety in depression. (epharmacygold.com)
  • Consumption of alcohol with this medicine may alter the effects of Amoxapine and cause serious side effects such as extreme drowsiness, confusion, vomiting, sweating, blurred vision, muscle stiffness, and seizures. (practo.com)
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  • Amoxapine is not recommended for use in patients taking monoamine oxidase inhibitors (MAOI) due to the increased risk of serious and life-threatening side effects. (practo.com)
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