Antidepresivos tricíclicos para los trastornos del espectro autista (TEA) en niños y adolescentes. Tricyclic Antidepressants for Autism Spectrum Disorders (ASD). Los antidepresivos son medicamentos que se cree que actúan cambiando las Antidepresivos tricíclicos (ATC); ejemplos son Elavil (amitriptilina), Tofranil. El riesgo potencial de los antidepresivos en relacion con el umbral convulsivo Deben evitarse el bupropion y los antidepresivos triciclicos.
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Tricyclic antidepressants TCAs are a class of medications that are used primarily as antidepressants. TCAs were discovered in the early s and were marketed later in the decade. Tetracyclic antidepressants TeCAswhich contain four rings of atoms, are a closely related group of antidepressant compounds. Although TCAs are sometimes prescribed for depressive disorders, they have been largely replaced in clinical use in most parts of the world by newer antidepressants such as selective serotonin reuptake inhibitors SSRIsserotonin—norepinephrine reuptake inhibitors SNRIs and norepinephrine reuptake inhibitors NRIs.
The TCAs are used primarily in the clinical treatment of mood disorders such as major depressive disorder MDDdysthymiaand treatment-resistant variants.
For many years the TCAs were the first choice for pharmacological treatment of clinical depression. Although they are still considered to be highly effectivethey have been increasingly replaced by antidepressants with an improved safety and side effect profile, such as the SSRIs and other newer antidepressants such as the novel reversible MAOI moclobemide. However, tricyclic antidepressants are possibly more effective in treating melancholic depression than other antidepressant drug classes.
Nonetheless, the TCAs are commonly prescribed for treatment-resistant depression that has failed to respond to therapy with newer antidepressants. The TCAs were used in the past in the clinical treatment of ADHD,  though they are not typically used anymore, having been replaced by more effective agents with fewer side effects such as atomoxetine Strattera, Tomoxetin and stimulants like methylphenidate Ritalin, Focalin, Concertaand amphetamine Adderall, Attentin, Dexedrine, Vyvanse.
ADHD is thought to be caused by an insufficiency of dopamine and norepinephrine activity in the prefrontal cortex of the brain. The TCAs show efficacy in the clinical treatment of a number of different types of chronic painnotably neuralgia or neuropathic pain and fibromyalgia. They may also be effective to prevent chronic tension headaches.
Many side effects may be related to the antimuscarinic properties of the Sntidepresivos. Twitching, hallucinations, delirium and coma are also some of the toxic effects caused by overdose. Tolerance to these adverse effects of these drugs often develops if treatment is continued.
Side effects may also be less troublesome if treatment is initiated with low doses and then gradually increased, although this may also delay the beneficial effects.
TCAs can behave like class 1A triciclicksas such, they can theoretically terminate antidepreisvos fibrillation, decrease cardiac contractility and increase collateral blood circulation to ischemic heart muscle. Naturally, in overdose, they can be cardiotoxic, prolonging heart rhythms and increasing myocardial irritability. New research has also revealed compelling evidence of a link between long-term use of anticholinergic medications like TCAs and dementia. In the brain, acetylcholine is involved in learning and memory.
Antidepressants in general may produce a withdrawal. However, since the term “withdrawal” has been linked to addiction to recreational drugs like opioids, the antideprresivos profession and pharmaceutical public relations prefer that a different term be used, hence “discontinuation syndrome.
TCA overdose is a significant cause of fatal drug poisoning. The severe morbidity and mortality associated with these drugs is well documented due to their cardiovascular and neurological toxicity.
Additionally, it is a serious problem in the pediatric population due to their inherent toxicity  and the availability of these in the home when prescribed for bed-wetting and depression. In the event of a known or suspected overdose, medical assistance should be sought immediately.
An overdose on TCA is especially fatal as it is rapidly absorbed from the GI tract in the alkaline conditions of the small trciclicos.
As a result, toxicity often becomes apparent in the first hour after an overdose. However, symptoms may take several hours to appear if a mixed overdose has caused delayed gastric emptying.
Many of the initial signs are those associated to the anticholinergic effects of Antideprfsivos such as dry mouth, blurred vision, urinary retention, constipation, dizziness, and emesis or vomiting. Due to the location of norepinephrine receptors all over the body, many physical signs are also associated with a TCA overdose: Initially, gastric decontamination of the patient is achieved by administering, either orally or via a nasogastric tubeactivated charcoal pre-mixed with water, which adsorbs the drug in the gastrointestinal tract most useful if given within 2 hours of drug ingestion.
If there is metabolic acidosis, intravenous infusion of sodium bicarbonate is recommended by Toxbase. The TCAs are highly metabolised by the cytochrome P hepatic enzymes.
[Antidepressants in epilepsy].
Drugs that inhibit cytochrome P for example cimetidinemethylphenidatefluoxetineantipsychoticsand calcium channel blockers may produce decreases in the TCAs’ metabolism, leading to increases in their blood concentrations and accompanying toxicity.
Side effects may also be enhanced by other drugs that have antimuscarinic properties. The majority of the TCAs act primarily as SNRIs by blocking the serotonin transporter SERT and the norepinephrine transporter NETrespectively, which results in an elevation of the synaptic concentrations of these neurotransmittersand therefore an enhancement of neurotransmission.
These properties are often beneficial in antidepressants, especially with comorbid anxiety, as it provides a sedative effect. Most, if not all, of the TCAs also potently inhibit sodium channels and L -type calcium channelsand therefore act as sodium channel blockers and calcium channel blockersrespectively.
In summary, tricyclic antidepressants can acts through NMDA antagonism, opioidergic effects, sodium, potassium and calcium channel blocking, through interfering with the reuptake of serotonin, and acting as antagonists to SHAM serotonin, histamine, alpha, muscarinic receptors. Thus their dangerous side effect profile limits their use in daily practice. The binding profiles of various TCAs and some metabolites in terms of their affinities K inM for various receptors and transporters are as follows: With the exception of the sigma receptorsthe TCAs act as antagonists or inverse agonists of the receptors and as inhibitors of the transporters.
Tianeptine is included in this list due to it technically being a TCA, but with a vastly different pharmacology. The TCAs were developed amid the “explosive birth” of psychopharmacology in the early s. The first widely used psychiatric drug, by it was already generating significant revenue as an antipsychotic. The first TCA reported for the treatment of depression was imipraminea dibenzazepine analogue of chlorpromazine code-named G It was not originally targeted for the treatment of depression.
The drug’s tendency to induce manic effects was “later described as ‘in some patients, quite disastrous'”. The paradoxical observation of a sedative inducing mania led to testing with depressed patients.
The first trial of imipramine took place in and the first report of antidepressant effects was published by Swiss psychiatrist Roland Kuhn in Dibenzazepine derivatives are described in U.
The compounds described share a tricyclic backbone different from the backbone of the TCA amitriptyline.
Merck introduced the second member of the TCA family, amitriptyline Elavilin A very small number of cases involving non-medical use of antidepressants have been reported over the past 30 years.
Several cases of the misuse  of amitriptyline alone   or together with methadone   or in other drug dependent patients   and of dosulepin with alcohol  or in methadone patients  have been reported. Those that preferentially inhibit the reuptake of serotonin by at least fold over norepinephrine include:. Those that preferentially inhibit the reuptake of norepinephrine by at least fold over serotonin include:.
Whereas either fairly balanced reuptake inhibitors of serotonin and norepinephrine or unspecified inhibitors include:. And the following are TCAs that act via main mechanisms other than serotonin or norepinephrine reuptake inhibition:. From Wikipedia, the free encyclopedia.
Tricyclic antidepressant Drug class Chemical structure of the prototypical and first marketed tricyclic antidepressant imipramine. Notice its three rings. Bolded names indicates products which are available in at least three countries in which English is an official language. Canadian Medical Association Journal. Glazener, Cathryn MA, ed. The place of the new antidepressants”.
J Occup Med Toxicol. Des Moines University Psychiatry Class. Tricyclic antidepressant exposure in toddlers”. British Journal of Pharmacology.
Cellular and Molecular Neurobiology. Annual Review of Pharmacology and Toxicology. European Journal of Pharmacology. The British Journal of Psychiatry. The Journal of Pharmacology and Experimental Therapeutics. The American Journal of Emergency Medicine. Cairns 1 September Peripheral Receptor Targets for Analgesia: Novel Approaches to Pain Management. Retrieved 14 August Ghose 11 November Antidepressants for Elderly People.
Meyler’s Side Effects of Psychiatric Drugs. Shorter Oxford Textbook of Psychiatry.
Antidepresivos: otra arma contra el dolor crónico – Mayo Clinic
Between Commerce and Civil Society. Drugs Of Abuse, 2nd Edition. National Library of Medicine. Abuse Potential of Common Psychiatric Medications”. The patient denied any alcohol or substance abuse, and no signs of withdrawal were noted in the hospital The patient expressed fears of being addicted to the amitriptyline and desired inpatient hospitalization for medication adjustment and education.
Indian J Med Sci. A, a year-old abuser of alcohol and cannabis, consulted her family physician because of anxiety, depression, and insomnia. Unaware of her drug abuse, he prescribed amitriptyline, mg. About 30 minutes after taking each dose, she would experience relief from her symptoms that lasted about 2 hours.
By increasing the dose, she found she could intensify these effects and prolong them for up to several hours. Frequently, this progressed to incoordination, slurred speech, and confusion. Tricyclic and tetracyclic antidepressants.