Depression protriptyline

Tricyclic Antidepressants (TCAs). TCAs were introduced in the 1950s and over the years have become the mainstay of treatment for cataplexy and the other REM-related symptoms. The doses used are usually less than the doses required in the treatment of depression. Imipramine (Tofranil) is the most widely used TCA for narcolepsy and is usually effective at doses from 10 to 75 mg given once a day. Some doctors prefer the TCA protriptyline (Vivactil) because it has mild stimulant effects, but it has not been as widely used or as thoroughly studied in narcolepsy. The common side effects of TCAs are drowsiness, dry mouth, and constipation, but these are usually not a problem at the lower doses used for narcolepsy. Patients should receive a baseline electrocardiograph (EKG) before starting a TCA and should have blood levels of the medication checked periodically. 

Protriptyline is a powerful antidepressant, the mechanism of action of which is not known. It is not a MAO inhibitor and does not stimulate the CNS. It begins to act much faster and acts much longer than imipramine or amitriptyline. Protriptyline does not possess sedative tranquilizing properties. It is used in clinical conditions for treating severe depression. The most common synonyms are concordin, triptil, and vivactil. 

Relief of symptoms of depression (except clomipramine). The activating properties of protriptyline make it particularly suitable for withdrawn and anergic patients. Agents with significant sedative action may be useful in depression associated with anxiety and sleep disturbances. The activating properties of protriptyline make it particularly suitable for withdrawn and anergic patients. 

Seven TCA drugs are available in the United States for treatment of major depression. They are generally categorized as tertiary or secondary amines. Tertiary amines include imipramine (Tofranil), amitriptyline (Elavil), trimipramine (Surmontil), and doxepin (5m-equan). Desipramine (Norpramin), nortriptyline (Pam-elor), and protriptyline (Vivactil) are secondary amines. 

Jitteriness, tachycardia, and tremor can occur early in the course of treatment, particularly in patients with co-morbid panic attacks. TCAs may cause a persistent, fine, rapid tremor, particularly in the upper extremities. Desipramine and protriptyline may be the most common offenders. Propranolol (60 mg per day) may help and is unlikely to worsen depression. Alternatively, switching to a drug with less NE activity may also help. 

Utilizing platelets from depressed patients, it was shown 32 that a significant reduction in mean 5-HT and DA uptake occurred in endogenously depressed patients but not in neurotic depressives. In this same study 32 it was reported that chlorimipramine caused a rapid reduction in 5-HT uptake, whereas protriptyline administration had no effect. 

Clinically, protriptyline is a purer type of antidepressant agent, in that it lacks the sedative properties of amitriptyline and nortriptyline. It is said to be the more potent of the three agents and useful also in the treatment of anxiety depressions. However, until further clinical work is published, it will be difficult to assess the therapeutic spectrum of this most recent agent. 

The dibenzapine derivatives are called tricyclic antidepressants and include imipramine (Tofranil), desipramine (Norpramin), amitriptyline (Elavil), nortriptyline (Aventyl), protriptyline (Vivactil), and doxepin (Adapin). Amitriptyline is indicated in depression major depression with melancholia or psychotic symptoms depressive phase of bipolar disorder depression associated with organic disease, alcoholism, schizophrenia, or mental retardation anorexia or bulimia associated with depression (see Figure 20). 

Protriptyline, a tricyclic antidepressant (15 to 40 mg p.o. daily), is used in the treatment of depression (see also Tables 5 through 7). 

These drugs are used to alleviate depression, and are also used in the therapy of diabetic neuropathy. They may also be effective in the treatment of obsessive compulsive disorder (OCD) and attention-deficit hyperactivity disorder. Certain drugs of this class have also been therapeutically useful in the treatment of childhood enuresis (e.g., imipramine), fibromyalgia (e.g., amitriptyline), and chronic obstructive pulmonary disease (COPD) (e.g., protriptyline). 

Antidepressants with sedation as a side effect often are used to treat insomnia. The antidepressants most frequently associated with sedation as a side effect are the tricyclics (amitryptyline, imipramine, nortriptyline, trimipramine, doxepin, amoxapine, and protriptyline), nontricyclics (maprotiline and mirtazepine), trazodone, and nefazodone (55), which are discussed in greater detail in Chapter 21. Of these drugs, trazodone, doxepin, and mirtazepine have been shown to be effective in the treatment of insomnia in patients with depression (1). The effectiveness of these drugs to treat insomnia in nondepressed patients, however, has not been proven. The mechanism by which this occurs is unknown, but most of these drugs have some activity as H2 antagonists that may contribute to the effect (56). 

Sham rage produced by brain stem transection in cats is accompanied by changes in brain stem norepinephrine. Rage is increased by protriptyline that increases the action of norepinephrine, and by haloperidol that depresses its action. 

Tricyclics are the most commonly prescribed drag to treat major depression. Tricyclics include clomipramine HCl (Anafranil), desipramine HCl (Norpramin, Pertofrane), doxepin HCl (Sinequan), imipramine HCl (Tofranil), NortriptyMne HCl (Aventyl), Protriptyline HCl (Vivactil), and trimipramine maleate (Surmontil). 

Part of the explanation for the increased C3S1S depression is that both alcohol and some of the tricyclics, particularly amitriptyline, cause drowsiness and other CNS depressant effeets, which can be additive with the effects of alcohol. The sedative effects have been reported to be greatest with amitriptyline, then doxepin and imipramine, followed by nortriptyline, and least with amoxapine, clomipramine, desipramine, and protriptyline. In addition acute alcohol intake causes marked increases (100 to 200%) in the plasma levels of amitriptyline, probably by inhibiting its first pass metabolism. Alcohol-induced liver damage could also result in impaired amitriptyline metabolism. The lower serum levels of imipramine and desipramine seen in abstinent alcoholics are attributable to induction of the cytochrome P450 isoenzymes by alcohol. ... 

---