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• W4244545900 abstract "Therapeutic Reviews aim to provide essential independent information for health professionals about drugs used in palliative and hospice care. Additional content is available on www.palliativedrugs.com. Country-specific books (Hospice and Palliative Care Formulary USA, and Palliative Care Formulary, British and Canadian editions) are also available and can be ordered from www.palliativedrugs.com. The series editors welcome feedback on the articles ([email protected]). Therapeutic Reviews aim to provide essential independent information for health professionals about drugs used in palliative and hospice care. Additional content is available on www.palliativedrugs.com. Country-specific books (Hospice and Palliative Care Formulary USA, and Palliative Care Formulary, British and Canadian editions) are also available and can be ordered from www.palliativedrugs.com. The series editors welcome feedback on the articles ([email protected]). 5-hydroxytryptamine-1A, -2, and -3 receptors, etc. Alpha, alpha-1 and -2 receptors Anticholinergic (muscaric) receptor Amyotrophic lateral sclerosis/motor neuron disease Bis in die, twice daily Cognitive behavioral therapy Central nervous system Cytochrome P450 Dopamine-2 receptor Dopamine Diagnostic and Statistical Manual of Mental Disorders Electrocardiogram Gamma-aminobutyric acid Gastrointestinal Histamine-1 receptor Intramuscular Intravenous Monoamine oxidase inhibitor Monoamine re-uptake inhibitor Norepinephrine and dopamine re-uptake inhibitor Norepinephrine (noradrenaline) National Institute for Health and Clinical Excellence N-methyl-D-aspartate Number needed to harm, i.e., the number of patients needed to be treated in order to harm one patient sufficiently to cause withdrawal from a drug trial Per os, by mouth Pro re nata, as needed Every 2 hours, 6 hours, etc. Receptor antagonist Randomized controlled trial Subcutaneous Serotonin and norepinephrine re-uptake inhibitor Selective serotonin re-uptake inhibitor Tricyclic antidepressant Ter in die, three times daily Time to reach maximum plasma concentration Indications: Depression, anxiety and panic disorders, post-traumatic stress disorder, stress incontinence and urgency, †chronic pain, †agitated delirium, †sweating, †hot flashes, †insomnia, †pruritus, †bladder spasm, †pathological laughing and crying, †drooling. Depression: Antidepressants enhance transmission of one or more monoamines (Fig. 1, Box 1). Some have additional actions which may contribute towards their beneficial and/or undesirable effects (Table 1). Although increased monoamine transmission occurs within hours, the antidepressant effect is slower to appear because this requires normalization of receptor sensitivity and neuroplasticity. Many of the early-onset undesirable effects from antidepressant drugs are a consequence of enhanced monoamine transmission in the presence of receptors that have been upregulated to compensate for a relative monoamine deficit. As receptor sensitivity returns to normal, these undesirable effects generally resolve and beneficial effects begin to emerge.Box 1Classification of Antidepressants According to Principal ActionsaMonoamine re-uptake inhibitors (MARIs) Serotonin and norepinephrine (SNRIsb or dual inhibitors)Amitriptylinec, venlafaxine, duloxetine Serotonin (selective serotonin re-uptake inhibitors, SSRIs)Sertraline, citalopram, paroxetine, fluoxetine Norepinephrine (NRIs)Nortriptylinec, lofepramine, desipraminec, reboxetine Norepinephrine and dopamine (NDRIs)BupropionPsychostimulant-antidepressantsd Dextroamphetamine, methylphenidate, modafinilReceptor antagonists Trazodone (α1, 5HT2) Mirtazapine (central α2, 5HT2, 5HT3)Monoamine oxidase inhibitors (MAOIs)e Phenelzine, tranylcypromineaAbbreviated names broadly reflect those found elsewhere;15Stahl S.M. Psychosis and schizophrenia.in: Stahl S.M. Essential psychopharmacology: Neuroscientific basis and practical applications. 3rd ed. Cambridge University Press, New York2008: 247-325Google Scholar confusion is inevitable because S is used for Selective, Specific, and Serotonin.bSNRI is sometimes reserved for dual inhibitors without additional receptor binding affinities (e.g., venlafaxine and duloxetine).cTCAs differ in their modes of action, and do not comprise a single discrete drug class.dReverse dopamine re-uptake transporters.eMAOIs are included for completeness; their use by non-psychiatrists is not recommended.Table 1Transporter and Receptor Affinities for Selected Antidepressants16National Institute of Mental Health (NIMH). (2006) NIMH's psychoactive drug screening program. Available from http://pdsp.med.unc.edu. Accessed August 2012.Google Scholar, 17Stahl S.M. Pradko J.F. Haight B.R. et al.A review of the neuropharmacology of bupropion, a dual norepinephrine and dopamine reuptake inhibitor.Prim Care Companion J Clin Psychiatry. 2004; 6: 159-166Crossref PubMed Google Scholar, 18Béïque J.C. Lavoie N. de Montigny C. Debonnel G. Affinities of venlafaxine and various reuptake inhibitors for the serotonin and norepinephrine transporters.Eur J Pharmacol. 1998; 349: 129-132Crossref PubMed Scopus (88) Google Scholar, 19Hamon M. Bourgoin S. Pharmacological profile of antidepressants: a likely basis for their efficacy and side effects?.Eur Neuropsychopharmacol. 2006; 16: s625-s632Abstract Full Text PDF Scopus (31) Google ScholarDrugRe-uptake TransportersReceptor Affinities5HTNEaThe norepinephrine re-uptake transporter also clears dopamine in the prefrontal cortex where dopamine re-uptake transporters are absent. Reduced dopamine in the prefrontal cortex is related to anhedonia and inattention.DA5HT2A5HT2CH1α1α2AChMAgomelatine (not USA)bAgomelatine is also a melatonin (type 1 and 2) receptor agonist. Although animal models raise this as a target of possible interest, the contribution which this makes towards its clinical effects in humans is unclear.-+---Amitriptyline+++++-++++++++++++++++Bupropion-+++-----Citalopram+++--------Desipramine++++-+-++++-+Duloxetine+++++++------Fluoxetine+++--++----Imipramine++++-+++++++-+/+++cVaries with different AChM receptor subtypes.Lofepramine (not USA)++++--++--/++cVaries with different AChM receptor subtypes.Methylphenidate--++-----Mirtazapine---+++++++-+++-Nortriptyline++++-+++++++++++-++Paroxetine++++------+Reboxetine (not USA)-+++-----Sertraline+++-+---+--Trazodone---+++-+++-Venlafaxine++dDespite in vitro studies suggesting a relatively low affinity for serotonin and norepinephrine re-uptake transporters, in vivo studies suggest venlafaxine is a dual inhibitor. In vitro assays measure the ability of a drug to displace another compound of known affinity; it may be that venlafaxine binds to a different site on monoamine re-uptake transporters and so cannot displace the reference compounds.18-------Affinity=+++ high, ++ moderate, + low, - negligible or none; blank=no data.a The norepinephrine re-uptake transporter also clears dopamine in the prefrontal cortex where dopamine re-uptake transporters are absent. Reduced dopamine in the prefrontal cortex is related to anhedonia and inattention.b Agomelatine is also a melatonin (type 1 and 2) receptor agonist. Although animal models raise this as a target of possible interest, the contribution which this makes towards its clinical effects in humans is unclear.c Varies with different AChM receptor subtypes.d Despite in vitro studies suggesting a relatively low affinity for serotonin and norepinephrine re-uptake transporters, in vivo studies suggest venlafaxine is a dual inhibitor. In vitro assays measure the ability of a drug to displace another compound of known affinity; it may be that venlafaxine binds to a different site on monoamine re-uptake transporters and so cannot displace the reference compounds.18Béïque J.C. Lavoie N. de Montigny C. Debonnel G. Affinities of venlafaxine and various reuptake inhibitors for the serotonin and norepinephrine transporters.Eur J Pharmacol. 1998; 349: 129-132Crossref PubMed Scopus (88) Google Scholar Open table in a new tab Monoamine re-uptake inhibitors (MARIs) Serotonin and norepinephrine (SNRIsb or dual inhibitors) Amitriptylinec, venlafaxine, duloxetine Serotonin (selective serotonin re-uptake inhibitors, SSRIs) Sertraline, citalopram, paroxetine, fluoxetine Norepinephrine (NRIs) Nortriptylinec, lofepramine, desipraminec, reboxetine Norepinephrine and dopamine (NDRIs) Bupropion Psychostimulant-antidepressantsd Dextroamphetamine, methylphenidate, modafinil Receptor antagonists Trazodone (α1, 5HT2) Mirtazapine (central α2, 5HT2, 5HT3) Monoamine oxidase inhibitors (MAOIs)e Phenelzine, tranylcypromine aAbbreviated names broadly reflect those found elsewhere;15Stahl S.M. Psychosis and schizophrenia.in: Stahl S.M. Essential psychopharmacology: Neuroscientific basis and practical applications. 3rd ed. Cambridge University Press, New York2008: 247-325Google Scholar confusion is inevitable because S is used for Selective, Specific, and Serotonin. bSNRI is sometimes reserved for dual inhibitors without additional receptor binding affinities (e.g., venlafaxine and duloxetine). cTCAs differ in their modes of action, and do not comprise a single discrete drug class. dReverse dopamine re-uptake transporters. eMAOIs are included for completeness; their use by non-psychiatrists is not recommended. Affinity=+++ high, ++ moderate, + low, - negligible or none; blank=no data. Neuroplasticity is the ability of the CNS to adapt structurally and functionally in response to external stimuli and is mediated by nerve growth factors (e.g., brain derived neurotrophic factor). In depression, neuroplasticity is impaired in the limbic and prefrontal cortex circuits which regulate mood, attention, energy, appetite and sleep. By enhancing monoamine transmission, antidepressants help increase the production of nerve growth factors and restore neuroplasticity.1Castren E. Rantamaki T. Role of brain-derived neurotrophic factor in the aetiology of depression: implications for pharmacological treatment.CNS Drugs. 2010; 24: 1-7Crossref PubMed Scopus (44) Google Scholar Depression refractory to one antidepressant can respond following a switch to another antidepressant or to the use of combination treatment which targets different, or multiple, monoamines (see Titrating, switching and combining antidepressants).2Belmaker R.H. Agam G. Major depressive disorder.N Engl J Med. 2008; 358: 55-68Crossref PubMed Scopus (456) Google Scholar, 3Tran P.V. Bymaster F.P. McNamara R.K. Potter W.Z. Dual monoamine modulation for improved treatment of major depressive disorder.J Clin Psychopharmacol. 2003; 23: 78-86Crossref PubMed Scopus (104) Google Scholar Anxiety and Panic Disorder: Antidepressants and benzodiazepines inhibit the amygdala's so-called fear circuits through 5HT1A and GABAA receptors, respectively.4Akimova E. Lanzenberger R. Kasper S. The serotonin-1A receptor in anxiety disorders.Biol Psychiatry. 2009; 66: 627-635Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar, 5Maron E. Shlik J. Serotonin function in panic disorder: important, but why?.Neuropsychopharmacology. 2006; 31: 1-11Crossref PubMed Google Scholar The amygdala is a “threat sensor” which integrates sensory information with contextual information (e.g., interpretations, memories). If a fear response is required, the amygdala's effector pathway activates the relevant circuits (respiratory and cardiovascular centers, pituitary-adrenal axis, sympathetic autonomic nervous system, and fear-related areas of the cerebral cortex). Pain: The analgesic effects of antidepressants also are due to enhanced monoamine transmission, e.g., in descending pain modulation pathways.6Nickel F.T. Seifert F. Lanz S. Maihöfner C. Mechanisms of neuropathic pain.Eur Neuropsychopharmacol. 2012; 22: 81-91Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar, 7McCleane G. Antidepressants as analgesics.CNS Drugs. 2008; 22: 139-156Crossref PubMed Scopus (32) Google Scholar These pathways can induce both analgesia (norepinephrinergic (noradrenergic) and serotoninergic activity) and hyperalgesia (serotoninergic activity).8Heinricher M.M. Tavares I. Leith J.L. Lumb B.M. Descending control of nociception: specificity, recruitment and plasticity.Brain Res Rev. 2009; 60: 214-225Crossref PubMed Scopus (213) Google Scholar, 9Dogrul A. Ossipov M.H. Porreca F. Differential mediation of descending pain facilitation and inhibition by spinal 5HT-3 and 5HT-7 receptors.Brain Res. 2009; 1280: 52-59Crossref PubMed Scopus (73) Google Scholar The latter may explain the inconsistent analgesic effect of SSRIs and why SNRIs appear no more effective then NRIs.10Watson C.P. Vernich L. Chipman M. Reed K. Nortriptyline versus amitriptyline in postherpetic neuralgia: a randomized trial.Neurology. 1998; 51: 1166-1171Crossref PubMed Google Scholar Sodium-channel blockade and NMDA-glutamate-receptor antagonism also may contribute to the analgesic efficacy of some antidepressants,7McCleane G. Antidepressants as analgesics.CNS Drugs. 2008; 22: 139-156Crossref PubMed Scopus (32) Google Scholar including the modest effect of topical doxepin.11McCleane G. Topical application of doxepin hydrochloride, capsaicin and a combination of both produces analgesia in chronic human neuropathic pain: a randomized, double-blind, placebo-controlled study.Br J Clin Pharmacol. 2000; 49: 574-579Crossref PubMed Scopus (115) Google Scholar, 12McCleane G.J. Topical doxepin hydrochloride reduces neuropathic pain: a randomised, double-blind, placebo-controlled study.Pain Clinic. 2000; 12: 47-50Crossref Google Scholar The beneficial and undesirable effects of antidepressants vary for multiple reasons including differing:•mechanisms of action (Fig. 1)•monoamines affected (Box 1)•effects on other receptors (Table 1)•pharmacokinetic profiles (Table 2).Table 2Pharmacokinetic Details for Selected Antidepressants20Wen B. Ma L. Rodrigues A.D. Zhu M. Detection of novel reactive metabolites of trazodone: evidence for CYP2D6-mediated bioactivation of m-chlorophenylpiperazine.Drug Metab Dispos. 2008; 36: 841-850Crossref PubMed Scopus (28) Google Scholar, 21Jefferson J.W. Pradko J.F. Muir K.T. Bupropion for major depressive disorder: pharmacokinetic and formulation considerations.Clin Ther. 2005; 27: 1685-1695Abstract Full Text PDF PubMed Scopus (83) Google Scholar, 22Hiemke C. Härtter S. Pharmacokinetics of selective serotonin reuptake inhibitors.Pharmacol Ther. 2000; 85: 11-28Crossref PubMed Scopus (373) Google Scholar, 23Fleishaker J.C. Clinical pharmacokinetics of reboxetine, a selective norepinephrine reuptake inhibitor for the treatment of patients with depression.Clin Pharmacokinet. 2000; 39: 413-427Crossref PubMed Google Scholar, 24Venkatakrishnan K. Greenblatt D.J. von Moltke L.L. et al.Five distinct human cytochromes mediate amitriptyline N-demethylation in vitro: dominance of CYP 2C19 and 3A4.J Clin Pharmacol. 1998; 38: 112-121Crossref PubMed Google Scholar, 25Richelson E. Pharmacokinetic drug interactions of new antidepressants: a review of the effects on the metabolism of other drugs.Mayo Clin Proc. 1997; 72: 835-847Abstract Full Text Full Text PDF PubMed Google Scholar, 26Kaye C.M. Haddock R.E. Langley P.F. et al.A review of the metabolism and pharmacokinetics of paroxetine in man.Acta Psychiatr Scand Suppl. 1989; 350: 60-75Crossref PubMed Google Scholar, 27Schulz P. Dick P. Blaschke T.F. Hollister L. Discrepancies between pharmacokinetic studies of amitriptyline.Clin Pharmacokinet. 1985; 10: 257-268Crossref PubMed Google Scholar, 28Abernethyl D.R. Divoll M. Greenblatt D.J. Harmatz J.S. Shader R.I. Absolute bioavailability of imipramine: influence of food.Psychopharmacology (Berl). 1984; 83: 104-106Crossref PubMed Scopus (8) Google ScholarDrugBio-availability PO (%)Tmax (h)Plasma Half-life (h)MetabolismAgomelatine (not USA)>801–21–2CYP1A2aSignificant first-pass metabolism.Amitriptyline45413–36Multiple pathwaysbActive metabolite(s); listed in table if can be administered separately. (nortriptylinebActive metabolite(s); listed in table if can be administered separately.)Bupropion>871.521CYP2B6bActive metabolite(s); listed in table if can be administered separately.Citalopram80cTablet product: bioavailability of drops 25% higher.336Multiple pathwaysbActive metabolite(s); listed in table if can be administered separately.Desipramine30–504–67–77CYP 2D6aSignificant first-pass metabolism.,bActive metabolite(s); listed in table if can be administered separately.Duloxetine90612CYP1A2, CYP2D6Fluoxetine904–81–4 days 7–15 daysbActive metabolite(s); listed in table if can be administered separately.Multiple pathwaysbActive metabolite(s); listed in table if can be administered separately.Imipramine45321Multiple pathwaysbActive metabolite(s); listed in table if can be administered separately. (desipraminebActive metabolite(s); listed in table if can be administered separately.)Methylphenidate301–32Non-CYP hepatic carboxylesteraseaSignificant first-pass metabolism.Mirtazapine50220–40CYP1A2, CYP2D6, CYP3A4Nortriptyline607–8.515–39CYP2D6aSignificant first-pass metabolism.,bActive metabolite(s); listed in table if can be administered separately.Paroxetine50dIncreases with multiple dosing.515–20Multiple pathwaysReboxetine (not USA)952–412CYP3A4Sertraline>446–826CYP3A4Trazodone6517CYP2D6, CYP3A4bActive metabolite(s); listed in table if can be administered separately.Venlafaxine13 (45)em/r product.2.5 (4.5–7.5)em/r product.5 (11)bActive metabolite(s); listed in table if can be administered separately.CYP2D6, CYP3A4bActive metabolite(s); listed in table if can be administered separately.a Significant first-pass metabolism.b Active metabolite(s); listed in table if can be administered separately.c Tablet product: bioavailability of drops 25% higher.d Increases with multiple dosing.e m/r product. Open table in a new tab The clearance of many antidepressants is significantly affected by CYP2D6 metabolizer phenotype, and to a lesser extent by CYP2C19. Further, serotonin re-uptake transporter polymorphisms may influence SSRI efficacy.13Porcelli S. Fabbri C. Serretti A. Meta-analysis of serotonin transporter gene promoter polymorphism (5-HTTLPR) association with antidepressant efficacy.Eur Neuropsychopharmacol. 2012; 22: 239-258Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar However, clinical benefit from genotyping has yet to be demonstrated.14Kirchheiner J. Rodriguez-Antona C. Cytochrome P450 2D6 genotyping: potential role in improving treatment outcomes in psychiatric disorders.CNS Drugs. 2009; 23: 181-191Crossref PubMed Scopus (19) Google Scholar St. John's wort (hypericum extract) is as effective as conventional antidepressants in treating mild–moderate depression and causes fewer undesirable effects.29Linde K. Berner M.M. Kriston L. St. John's wort for major depression.Cochrane Database Syst Rev. 2008; 4: CD000448PubMed Google Scholar However, NICE discourages its use because of:•uncertainty about appropriate doses•variation in the nature of products•potential serious interactions with other drugs (including oral contraceptives, anticoagulants and anti-epileptics).30National Institute for Health and Clinical Excellence (NICE). Clinical guidleline 90 and 91. Depression. 2009. Available from www.nice.org.uk. Accessed August 2012.Google Scholar In patients with a history of mania, antidepressants may precipitate a recurrent episode, particularly when administered without a mood stabilizer. The risk of antidepressant-related suicidal ideation needs to be balanced against the greater risk of non-fatal self harm and completed suicide from untreated depression.31Freeman S.A. Suicide risk and psychopharmacology: assessment and management of acute and chronic risk factors.J Clin Psychiatry. 2009; 70: 1052-1053Crossref PubMed Scopus (2) Google Scholar One in 1,000 patients attempt suicide in the six months after starting antidepressants: one-third are successful.32Simon G.E. Savarino J. Operskalski B. Wang P.S. Suicide risk during antidepressant treatment.Am J Psychiatry. 2006; 163: 41-47Crossref PubMed Scopus (231) Google Scholar In those aged ≤25 years, antidepressants are associated with suicidal ideation and non-fatal self-harm (NNH 143).33Stone M. Laughren T. Jones M.L. et al.Risk of suicidality in clinical trials of antidepressants in adults: analysis of proprietary data submitted to US Food and Drug Administration.BMJ. 2009; 339: b2880Crossref PubMed Scopus (153) Google Scholar, 34Bridge J.A. Iyengar S. Salary C.B. et al.Clinical response and risk for reported suicidal ideation and suicide attempts in pediatric antidepressant treatment: a meta-analysis of randomized controlled trials.JAMA. 2007; 297: 1683-1696Crossref PubMed Scopus (436) Google Scholar The risk is greater with SSRIs than TCAs,35Martinez C. Rietbrock S. Wise L. et al.Antidepressant treatment and the risk of fatal and non-fatal self harm in first episode depression: nested case-control study.BMJ. 2005; 330: 389Crossref PubMed Google Scholar and is present even when an antidepressant is used for non-depressive illnesses.34Bridge J.A. Iyengar S. Salary C.B. et al.Clinical response and risk for reported suicidal ideation and suicide attempts in pediatric antidepressant treatment: a meta-analysis of randomized controlled trials.JAMA. 2007; 297: 1683-1696Crossref PubMed Scopus (436) Google Scholar In adults ≥25 years old, there is a smaller increase in the risk of non-fatal self-harm (NNH ca. 700), no increase in suicide or suicidal thoughts, and no difference between SSRIs and TCAs.35Martinez C. Rietbrock S. Wise L. et al.Antidepressant treatment and the risk of fatal and non-fatal self harm in first episode depression: nested case-control study.BMJ. 2005; 330: 389Crossref PubMed Google Scholar, 36Gunnell D. Saperia J. Ashby D. Selective serotonin reuptake inhibitors (SSRIs) and suicide in adults: meta-analysis of drug company data from placebo controlled, randomised controlled trials submitted to the MHRA's safety review.BMJ. 2005; 330: 385Crossref PubMed Google Scholar, 37Fergusson D. Doucette S. Glass K.C. et al.Association between suicide attempts and selective serotonin reuptake inhibitors: systematic review of randomised controlled trials.BMJ. 2005; 330: 396Crossref PubMed Google Scholar Suicidal ideation should be evaluated when treating depression in all age groups. Consider the safety in overdose of both the antidepressant and concomitant medicines. In both the USA and Europe, regulators have emphasized the need for close monitoring of adherence to treatment, treatment response, and emergence of thoughts of self-harm, particularly during the first month after starting an antidepressant, and to encourage patients to report to their doctor any deterioration in mood or behavior.38Medicines and Healthcare Products Regulatory Agency. (2007) Antidepressants: suicidal behaviour. Drug Safety Update 2007;1(1): 7–8. Available from http://www.mhra.gov.uk/Safetyinformation/DrugSafetyUpdate/CON079102. Accessed August 21, 2012.Google Scholar, 39Reeves R.R. Ladner M.E. Antidepressant-induced suicidality: an update.CNS Neurosci Ther. 2010; 16: 227-234PubMed Google Scholar Antidepressants cause a dose-dependent reduction in seizure threshold. The risk is lowest for SSRIs, higher with TCAs, and highest with clomipramine, bupropion and maprotiline.40Harden C.L. Goldstein M.A. Mood disorders in patients with epilepsy: epidemiology and management.CNS Drugs. 2002; 16: 291-302Crossref PubMed Google Scholar There are fewer data and less experience with mirtazapine and venlafaxine. In patients with epilepsy, antidepressants also may cause seizures by altering anti-epileptic drug levels as a result of a drug–drug interaction. Thus, citalopram is widely favored for use in patients with epilepsy because of the low risk of reduction in seizure threshold and lack of significant interactions with anti-epileptic drugs. Antidepressants also can cause seizures through hyponatremia. It is hard to quantify the risk of using low-dose TCAs for neuropathic pain in patients with previous seizures because the risk is dose-related and animal studies even suggest a possible anti-epileptic action at low doses.41Dailey J.W. Naritoku D.K. Antidepressants and seizures: clinical anecdotes overshadow neuroscience.Biochem Pharmacol. 1996; 52: 1323-1329Crossref PubMed Scopus (63) Google Scholar Epilepsy is associated with both mood disorders and psychosis. Symptoms may occur in between (inter-ictal), during (ictal), or in the days or weeks after (post-ictal) seizures. Optimization of anti-epileptic medication should be considered alongside antidepressant treatment, particularly for ictal and post-ictal mood-related symptoms.42Blumer D. Montouris G. Davies K. The interictal dysphoric disorder: recognition, pathogenesis, and treatment of the major psychiatric disorder of epilepsy.Epilepsy Behav. 2004; 5: 826-840Abstract Full Text Full Text PDF PubMed Scopus (82) Google Scholar Further, anti-epileptic drugs can cause (and treat) mood disorders: seek specialist advice if symptoms develop after their introduction or titration.40Harden C.L. Goldstein M.A. Mood disorders in patients with epilepsy: epidemiology and management.CNS Drugs. 2002; 16: 291-302Crossref PubMed Google Scholar SSRIs can worsen extrapyramidal symptoms because serotonin reduces nigrostriatal dopamine release via inhibitory 5HT2 receptors. However, the risk appears small; few RCTs report any worsening.43Skapinakis P. Bakola E. Salanti G. et al.Efficacy and acceptability of selective serotonin reuptake inhibitors for the treatment of depression in Parkinson's disease: a systematic review and meta-analysis of randomized controlled trials.BMC Neurol. 2010; 10: 49Crossref PubMed Scopus (27) Google Scholar SSRIs are thus still often used in preference to TCAs which can worsen autonomic dysfunction (α blockade) and cognitive impairment (AChM blockade). 5HT2 antagonist antidepressants might be expected to avoid serotonin-mediated exacerbations. In small pilot RCTs, Parkinsonian symptoms improved with nefazodone44Avila A. Cardona X. Martin-Baranera M. et al.Does nefazodone improve both depression and Parkinson disease? A pilot randomized trial.J Clin Psychopharmacol. 2003; 23: 509-513Crossref PubMed Scopus (46) Google Scholar but not mirtazapine.45Zhang LS, Chen ZM, Zhang P. Mirtazapine vs. fluoxetine in treatng Parkinson's disease with depression and anxiety. Medical Journal of Chinese People's Health 2006. DOI: CNKI: SUN:ZMYX.0.2006-2023-2001.Google Scholar Antiparkinsonian D2 agonists can themselves improve mood. In RCTs evaluating pramipexole for motor symptoms, mood and motivation also improved.46Leentjens A.F. Koester J. Fruh B. et al.The effect of pramipexole on mood and motivational symptoms in Parkinson's disease: a meta-analysis of placebo-controlled studies.Clin Ther. 2009; 31: 89-98Abstract Full Text PDF PubMed Scopus (56) Google Scholar Further, in an RCT, pramipexole was more effective than sertraline for depression in patients with Parkinson's disease.47Barone P. Scarzella L. Marconi R. et al.Depression/Parkinson Italian Study GroupPramipexole versus sertraline in the treatment of depression in Parkinson's disease: a national multicenter parallel-group randomized study.J Neurol. 2006; 253: 601-607Crossref PubMed Scopus (149) Google Scholar Included for general information. MAOIs are not recommended in palliative care. They can cause serious adverse events when prescribed concurrently with various other drugs. Seek advice from a psychiatrist if caring for a patient already receiving an MAOI; their previous mental illness is likely to have been difficult to treat and switching or adding other psychotropics is difficult and risky. MAOIs are potentially dangerous because of the risk of serious dietary and drug interactions. Hypertensive crises are mainly associated with the consumption of tyramine-containing foods (Table 3). Typically, the patient experiences severe headache, and may suffer an intracranial hemorrhage. Drug interactions occur with sympathomimetics (e.g., ephedrine, pseudoephedrine, dextroamphetamine, nefopam), serotoninergics (see below) and levodopa.Table 3Tyramine-Containing Foods Associated With MAOI-Related SyndromeAlcoholFava Beans Red wine (white wine is safe)Meat (smoked or pickled) BeerMeat or yeast extractsBroad bean podsCheese (old)Pickled herring Open table in a new tab Toxicity has been reported with serotoninergic opioids (e.g., fentanils, meperidine [pethidine], tramodol). However, although pharmaceutical companies marketing morphine and oxycodone also advise against concurrent use, their affinity for the serotonin re-uptake transporter is negligible,48Gillman P.K. Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity.Br J Anaesth. 2005; 95: 434-441Crossref PubMed Scopus (179) Google Scholar and toxicity has not been reported.49Baxter K. Stockley's drug interactions (online edition). London: Pharmaceutical Press, 2011. Available from www.medicinescomplete.com. Accessed August 2012.Google Scholar Further, insisting on a two-week washout before treating pain is impracticable. MAOIs have numerous clinically significant drug interactions, which may result in hypertensive crises and serotonin toxicity. Several pharmacodynamic interactions (e.g., serotonin toxicity, bleeding risk, antimuscarinic effects, QT prolongation with citalopram and escitalopram) can be predicted from the mode of action of antidepressants (see Box 1 and Table 1). In addition, potentially serious interactions may result from induction or inhibition of hepatic metabolism. Some antidepressants inhibit cytochrome P450 enzymes:•CYP1A2 inhibition by fluvoxamine: e.g., tizanidine levels increased ≤33 times•CYP2D6 i" @default.
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• W4244545900 title "Antidepressant Drugs" @default.
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