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Desipramine side effects

Antidepressants are used in the treatment of neuropathic pain and headache. They include the classic tricyclic compounds and are divided into nonselective nor-adrenaline/5-HT reuptake inhibitors (e.g., amitriptyline, imipramine, clomipramine, venlafaxine), preferential noradrenaline reuptake inhibitors (e.g., desipramine, nortriptyline) and selective 5-HT reuptake inhibitors (e.g., citalopram, paroxetine, fluoxetine). The reuptake block leads to a stimulation of endogenous monoaminer-gic pain inhibition in the spinal cord and brain. In addition, tricyclics have NMDA receptor antagonist, endogenous opioid enhancing, Na+ channel blocking, and K+ channel opening effects which can suppress peripheral and central sensitization. Block of cardiac ion channels by tricyclics can lead to life-threatening arrhythmias. The selective 5-HT transporter inhibitors have a different side effect profile and are safer in cases of overdose [3]. [Pg.77]

Treatment with imipramine, the most studied TCA, leaves 45% to 70% of patients panic free. Both desipramine and clomipramine have demonstrated effectiveness in PD as well. Despite their efficacy, TCAs are considered second- or third-line pharmacotherapy due to poorer tolerability and toxicity on overdose.48,49 TCAs are associated with a greater rate of discontinuation from treatment than SSRIs.53 PD patients taking TCAs may experience anticholinergic effects, orthostatic hypotension, sweating, sleep disturbances, dizziness, fatigue, sexual dysfunction, and weight gain. Stimulant-like side effects occur in up to 40% of patients.49... [Pg.615]

Interaction with drug metabolism liquorices, which are the most commonly used herbs in TCM can increase metabolites (e.g., nortriptyline, desipramine, and norclomipramine) of tricyclic antidepressants (TCAs) and may produce more side effects (such as dry mouth, constipation, palpitation, etc.) (Xu, 2004 Zhu Huang, 2004). [Pg.121]

In 1985, 1 finally took the county public health psychiatrist s recommendation to try Desipramine, an ostensibly mild tricyclic antidepressant. I took tiny dot doses, and for a month or so I felt encouraged except for intense muscle tension and clenching. The psychiatrist said it was not remotely possible that this response was related to the medication. I took a low dose for four more months before throwing them out. The side effects had escalated horribly, and become what I later learned are called tardive dyskinesia and tardive dystonia. Subsequently, chemical and electromagnetic field exposures, feeling compromised or ashamed, or stress can trigger uncontrollable movement, hyperactivity, rigid posture and then, frequently, paralysis. [Pg.91]

The common side effects of TCAs frequently limit their usefulness, particularly in older patients. Side effects can be minimized by starting at low doses that are slowly titrated upward or by choosing one of the so-called secondary amine TCAs, nortriptyline and desipramine, with less potent side effects. In addition, it should be remembered that some of the troublesome side effects, such as sedation, tend to disappear over time. [Pg.52]

Tricyclic Antidepressants (TCAs). The TCAs, particularly imipramine (Tofranil), were also discovered soon after their introduction to be effective in the treatment of panic attacks. Imipramine, the best-studied TCA in the treatment of panic disorder, is most often helpful at daily doses of 150-250 mg, though it must be started at 10-25 mg, usually at bedtime, and gradually increased over 2-4 weeks. Although they are not as well studied, many clinicians prefer to use the secondary amine TCAs, desipramine (Norpramin) and nortriptyline (Pamelor), because they have milder side effects than imipramine. Clomipramine (Anafranil), though probably the TCA with the greatest side effect burden, is often said to be most effective in patients with refractory disease. [Pg.141]

Tricyclic Antidepressants (TCAs). Because of their effectiveness not only for depression but for anxiety disorders such as panic disorder as well, TCAs were the first medications formally tested in the treatment of PTSD. Three TCAs, amitriptyline, imipramine, and desipramine, have been studied in small trials, producing modest benefit for reexperiencing and hyperarousal symptoms, without any relief of avoidance/numbing symptoms. Given this limited benefit in conjunction with the side effect burden and potential for toxicity in a suicide prone population, TCAs are infrequently used in the treatment of PTSD. Please refer to Chapter 3 for more information regarding TCAs. [Pg.172]

Antidepressants. The tricyclic antidepressant desipramine has shown some small success in reducing cocaine craving, but the results are not overly impressive, and desipramine has many well-documented side effects and is dangerous in overdose (see Chapter 3 for more information). Cocaine-abusing patients who are not highly motivated will usually not remain adherent to the desipramine prescription. We do not recommend desipramine for the nondepressed cocaine addict. [Pg.198]

Tricyclic Antidepressants (TCAs). The TCAs have been nsed to treat ADHD for 30 or more years. Most often used are imipramine (Tofranil) and desipramine (Norpramin), mainly becanse they are the TCAs that most specihcally increase norepinephrine activity. Remember, boosting norepinephrine activity in the brain shonld improve attention. Other TCAs, namely, amitriptyline (Elavil, Endep) and nortriptyline (Pamelor), have been used, though they also increase norepinephrine activity. TCAs do offer a modest benefit for both the inattention and the hyperactivity of ADHD. In addition, they are often effective at doses mnch lower than those required to treat depression. However, their effectiveness nsnally falls short of the stimulant medications. In addition, TCAs have considerable side effects including dry mouth, constipation, drowsiness, weight gain, and adverse cardiac effects. [Pg.244]

Reboxetine is the only selective and reasonably potent noradrenaline reuptake inhibitor available clinically at the present time. Reboxetine has a chemical structure not dissimilar from viloxazine, an antidepressant which was of only limited clinical interest in the 1970s because of its weak efficacy and unacceptable side effects (nausea, vomiting and occasionally seizures). Unlike the secondary amine TCA antidepressants, such as maprotiline, desipramine, nortriptyline and protriptyline, reboxetine does not affect any other transporter or receptor system and therefore is largely devoid of TCA and SSRI-like side effects. In clinical trials, reboxetine has been shown to be as effective as the SSRIs in the... [Pg.175]

Pataki, C., Carlson, G., Kelly, K., and Rapport, M. (1993) Side effects of methylphenidate and desipramine alone and in combination in children./ Am Acad Child Adolesc Psychiatry 32 1065-1072. [Pg.262]

Tricyclic antidepressants (TCAs) modulate various brain neurotransmitters, especially norepinephrine and serotonin, by blocking reuptake presynaptically. The secondary amines (desipramine, nortriptyline) are more selective for noradrenergic function and have less side effects in sensitive populations. Advantages of this class of drugs include their relative long half life (approximately 12 hours), absence of abuse potential, and putative positive effects on mood and anxiety, sleep, and tics. [Pg.453]

Imipramine, amitriptyline, clomipramine, trimipramine, and doxepin are tertiary amine TCAs. Desipramine, nortriptyline, and protriptyline are secondary amine TCAs. Tertiary amine tricyclics have more potent serotonin reuptake inhibition, and secondary amine tricyclics have more potent noradrenergic reuptake inhibition. Tertiary amine TCAs tend to have more side effects than do... [Pg.41]

Imipramine, amitriptyline, doxepin, desipramine, clomipramine, and trimipramine therapy can be initiated at 25-50 mg/day. Divided dosing may be used at first to minimize side effects, but eventually the entire dose can be given at bedtime. The dose can be increased to 150 mg/day the second week, 225 mg/day the third week, and 300 mg/ day the fourth week. The dose of clomipramine should not exceed 250 mg/day because of an increased risk of seizures at higher doses. [Pg.42]

Besides being affected by medications and substances that affect the liver s metabolism, methadone itself affects the liver s metabolism of certain substances. A significant number of people who are taking methadone for heroin addiction also are HIV positive and are taking anti-HIV medications such as Desipramine (DMI) and zidovudine (AZT). Through its actions on the liver, methadone decreases the metabolism of these medications. Because of this, certain troublesome side effects of DMI and AZT, including nausea,... [Pg.329]

Helen P. is an obese 27-year-old woman who has been taking the antidepressant desipramine. She was started on a low dose and gradually increased to a dose of 300 mg daily, which she has been taking for the past three months. Even though Helen has only in the last two months been able to notice an effect, she now reports a significant improvement in her depression and no side effects. Her physician has forwarded results of periodic desipramine blood levels to you, and all are within therapeutic range. However, Helen recently discovered that a coworker also takes this medication, in a dose of 150 mg daily, and is doing well. [Pg.30]

Imipramine is the antidepressant most frequently prescribed for children and is the one most extensively studied in that population. Consider desipramine if anticholinergic side effects are to be avoided, for instance, in asthmatics. [Pg.205]

Reboxetine. Most of the activity of rehoxetine resides in the 5.5 isomer (The marketed compound is RR and 55.) It is claimed to he superior to fluoxetine in severe depression. It is marketed in Europe. At least three tricyclic compounds, desipramine. nortriptyline, and the technically tetracyclic maprotiline are SNERIs. They, of course, have typical characteristic TCA side effects but lower anticholinergic and H -antihistaminic (sedative) effects than dimethyl compounds. SNERIs arc clinically effective antidepressants. [Pg.519]

PertOfran desipramine. pertussis toxin (PTX) is elaborated by a bacterium Bordetella pertussis) and is a hexameric protein (4-5 subunits from A-B complex). It is a G-protein inactivator that binds to the ADP-ribosylation regulatory site of the G/Go family of subunits which couple negatively to adenylyl cyclase. The cellular responses blocked by PTX are varied, and typically include those due to 03 and opioid receptor type activation. The inactivation of this key regulatory unit explains some of the side-effects of whooping cough (caused by Bordetella pertussis) where production of this toxin is a main pathological factor. This toxin is an important pharmacological tool. [Pg.217]

Tricyclic antidepressants. (TCA) The anticholinergc side effects (dryness of mouth, constipation, increased sweating) associated with TCA (imipramine, desipramine) cause them to be poorly tolerated. They can only be recommended if other treatments have failed to reduce bingeing and/or purging. [Pg.61]


See other pages where Desipramine side effects is mentioned: [Pg.273]    [Pg.142]    [Pg.199]    [Pg.178]    [Pg.219]    [Pg.148]    [Pg.533]    [Pg.40]    [Pg.258]    [Pg.453]    [Pg.569]    [Pg.678]    [Pg.693]    [Pg.42]    [Pg.546]    [Pg.290]    [Pg.269]    [Pg.546]    [Pg.161]    [Pg.222]    [Pg.130]    [Pg.571]    [Pg.571]    [Pg.153]    [Pg.546]    [Pg.27]   
See also in sourсe #XX -- [ Pg.784 ]

See also in sourсe #XX -- [ Pg.784 ]




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Desipramine

Desipramine side effects profile

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