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Nefazodone is another important antidepressant drug that can inhibit 3A and can produce some potentially dangerous drug/drug interactions, again, you need to match this list to the proceeding list and go back and forth and you can make your own guesses about which one is doing what to whom.
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I think I want to move onto the clinical aspects of antidepressant drugs. The first probably most important thing to tell you about is that the effectiveness of the antidepressant drugs is one of the best kept scandals in our industry. The antidepressant drugs are good. I’m glad we’ve got them. They do wonderful things. I wouldn’t dare try practice trying to treat patients without them but to be quite honest about them they’re superiority to placebo is sometimes rather iffy. On average, if you want a kind of a rough number to keep in mind, about a third of people who meet the DSM-IV criteria for major depression will respond to a placebo within one to two months and about two-thirds, if you’re lucky, three-quarters will respond to an active drug. So the difference of drug and placebo is about a third of the action.
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Now some of that placebo response may include spontaneous remissions. One of the most important effects of major depression is that it is an episodic illness and if you can keep somebody alive and hopeful for nine months or a year, most people will recover spontaneously. It may well be that some of the variants of the placebo response is people coming in to treatment late in the illness and about to undergo a spontaneous remission. Anyway, the numbers that you see here show, again, this famous two-thirds/one-third rule and the difference is roughly 30% and this is what you’re betting on when you give any antidepressant.
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With ECT, the numbers are much better – a 90% ECT response, 10-20% placebo response. It’s better but it’s not perfect. With all these drugs – with the tricyclics, the SSRIs, MAO inhibitors, atypical drugs – the story is very similar and this kind of one_third/two-third rule sometimes, for example, with mirtazapine, it can be even less impressive but that’s the general rule of thumb in this field.
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So that leads to the quest for who’s the ideal candidate. That’s a very complicated story but rather quickly the story is if you have a classic endogenous melancholy, no-doubt- about-it depression is more likely to respond than a neurotic, questionable dysphoric kind of illness. If the severity is somewhere in the middle range, that is, people who have very mild but classic illnesses tend to respond questionably. People with very, very severe classic illnesses don’t respond as well so you have this kind of biphasic response versus severity relationship. So you have this two-dimensional story. There’s the type of illness – melancholy/non-melancholy is one dimension and then severity is another dimension.

Yet a third dimension is psychotic/nonpsychotic. Psychotic usually implies greater severity and one needs to tease apart the contributions of each and that has been done recently particularly by Jim Cosas at Cornell. The finding is that if you’re severe and psychotic you do rather poorly with any antidepressant, maybe better with ETC. Maybe a little bit better if you add a neuroleptic to an antidepressant.

Now, there are very similar analogous phenomena that are not as well worked out that seem to occur in the serotonin system whereby making more serotonin available by blocking its uptake. Autoreceptors for serotonin, again, desensitize and the serotonin system revs up and makes more transmitter available and some of the postsynaptic serotonin receptors analogous to alpha-1 in the adrenergic system remain available and do what has to be done.
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I’ve covered all this stuff and I think it’s time we cut to the chase and give you, again, kind of a bird’s eye summary. The story, again, is you can translate this, just change the name of the players but let’s say with the tricyclic antidepressants you block norepinephrine uptake and it stays knocked out indefinitely. As best as we know that makes more epinephrine available per unit time and per impulse and release and if mores available, does more. Paradoxically the system is designed to defeat the best efforts of the neuropharmacologist so what this really does is the presynaptic machinery turns itself off very quickly and you stop firing and you stop producing and you stop releasing norepinephrine and may actually get some sedative effects, hypertensive effects early on.
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But if you hold on for a week, two weeks, three weeks, the presynaptic alpha-2 autoreceptors become locked out, desensitized and the presynaptic machinery revs up and actually can go above baseline. So that by the time the drug is working out here at three or four weeks you still block the uptake, you’ve restored the presynaptic machinery to normal or more and you have retained sensitivity in the alpha-1 system postsynaptically to mediate the effects of the transmission.
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Beta fades out and that’s too bad. Some people used to speculate that loss of beta was the mechanism of action of antidepressant drugs. You ought to be aware of that because it may come up at a board exam but you could quote me and say, “If that were the case, then propranolol would be an excellent antidepressant” and just the opposite is the case. So I think this is a concomitant price of doing business probably. I don’t think that losing beta is necessarily the effect.

Just a word on drug disposition and pharmacokinetics and things of that kind and in the interest of time I really want to move onto more clinical topics. We know a good deal about the pharmacological half lives of these drugs. They vary considerably. Among the short acting are prazidone and bupropion. It’s one of the reasons that bupropion’s been reformulated into a sustained release. The same has happened with fexor, fentathizine has a short life of five hours and it too has been made into a long acting product.

Among the longest half life drugs are the secondary amine tricyclics and that would include drugs like, for example, protriptyline is very long acting. Probably the champion of longevity is the active byproduct of  Prozac, the demethylated Norflex which has a half life that’s not accurately known but it’s probably on the order of a week or more. So it means that that activity, and it’s biologically active, that drug will hang around for some weeks and if you start switching from Prozac to, God forbid, an MAO inhibitor or even a tricyclic antidepressant you can expect tricky problems to occur even a week or more after you stop the Prozac because of this long wash out time.

Now the serotonin system in the brain arises along the midline and under the nuclei that run down the stripe through the middle of the midbrain and brainstem called the raphe and the raphe system includes a number of clusters of nerve cells. The two most important are the dorsal and median raphe nuclei. Serotonin producing cells are located there. The median or the more posterior group sends motor neurons down to interact with the spinal cord anterior horn cells to facilitate and stimulate peripheral transmission to the motor end plate and the skeletal muscle system. Again, when this system gets revved up you can expect twitching and abnormal movements that are, again, seen in excessive serotonergic activity in the serotonin syndrome.

On the ascending group, the dorsal raphe system sends axons that go up into the hypothalamus limbic system and cortex, in fact, share some of the same pathways. For example, the median forebrain bundle is one of the hottest spots in the brain where if you stick a self stimulating electrode in the right brain in that area you can get animals to bar press for electrical stimulation in these systems that will go on until the cows come home. Rats will give up eating, drinking, sex, sleep, anything to be able to get more stimulation themselves in that forebrain bundle in this system. Not only the serotonin and noradrenergic systems going up to the limbic system but also the ascending dopaminergic systems are located there and all of these probably contribute in complicated ways to mediate affective states, drive states, behavioral reinforcements, and may underlie some addictive behaviors and probably are messed up in a very fundamental way, an important way in contributing to the biology of melancholic type of depressions.
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One of the other intriguing insights that I’ve alluded to already in passing is that many of these systems talk to each other. They’re not just working all by themselves but the adrenergic and serotonergic systems are actually crossing. One of the theories about the biology of the sleep/wake cycle and phases of sleep and circadian rhythms that make it difficult for people to lecture more than 60-90 minutes without a coffee break because attention flags and all these rhythmic activities of arousal and sleep and attention and many endocrine rhythms, temperature rhythms, other things that happen are regulated by hot point mechanisms that probably have to do with the circuitry down in the brainstem of these interactions.
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From a pharmacologic point of view these interactions have allowed some very interesting games to be played with drugs. For example, there are alpha-2 receptors sitting on the neuroterminals for the adrenergic system. They are among the most important of receptors to inhibit release of norepinephrine and alpha-2 antagonists tend to be mood elevating or stimulant. Drugs that stimulate these receptors tend to be antiadrenergic, lower blood pressure. Tend to be quieting behaviorally. May have mild antimanic effects and so on. There are also inhibitory agents that sit as heteroceptors on the serotonin axons and terminals. Again, if you block this effect, you’ll increase the release of serotonin and that may be one of the ways in which mirtazapine has its indirect effects on both adrenergic and serotonergic activity.
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Then the serotonin system has its own autoreceptors. Their nomenclature will keep shifting but there are autoreceptors and they tend to be modified with long term exposure to serotonin reuptake inhibitors. The alpha receptors up here, autoreceptors in the adrenergic system become modified, down-regulate, desensitize after long term exposure to the tricyclics. I’ll say more about that in a minute but these phenomena probably have a lot to do with the later equilibrium that’s established after treating with antidepressant drugs over many weeks when their clinical effects begin to come into play. There are also serotonin receptors, heteroceptors that sit on the adrenergic terminals. Again, drugs that block or facilitate these will have indirect effects on the adrenergic system. To give you a closeup view of a central, or peripheral for that matter, adrenergic terminal and this model actually serves very well for the serotonin system. There are enzymatic mechanisms that produce both serotonin and norepinephrine from precursor amino acids, tyrosine to dopa and dopamine to norepinephrine and the adrenergic system and tryptophan serotonin in the serotonin system.

Benzodiazepine tachyphylaxis: that’s a good one. Conventional, classic Board wisdom, the sleep tachyphylaxis happens very quickly, like in 2-6 weeks. First of all, why do we have 25 benzodiazepines, do we really need that many in the American market? In my opinion, the answer is no. You can order prozac 10 mg at our canadian pharmacy shop. They are all very similar. There are differences in how quickly they are absorbed. There are differences in the different sub-units. But by and large, there is a lot of similarity. Some of them though, I will admit, there are some genuine differences in that if they have a rapid onset of action they are better for sleep. A good example is triazolam, Halcion. That drug happens so fast, the onset is so fast, that you really can’t stay awake on it. I think it’s a lot of experiences of people, they will be sitting there drinking a glass of milk with their Halcion and they will fall asleep in their milk. They won’t even make it to bed. Contrast that with something like Clonopin which you can take at 8 o’clock in the morning and not fall asleep.  Why is that? I’ll tell you. With a lot of benzodiazepines what’s happening is this; you are getting a tachyphylaxis to the sleep after 4-6 weeks, but how come you still use it for sleep after three years? I’ll tell you why. Ativan, you take that at 4 o’clock. Do you feel sleepy? No, but you feel very relaxed. What happens if you take it at 12 ‘o clock? It doesn’t put you out like a Mickey Finn, but what happens is this: you are lying awake in bed, you are all wired up. You are thinking about the days events, about tomorrow. Suddenly you take that Ativan and you are very relaxed and sleep takes over naturally. So I think what happens is that it is still useful for sleep, even though the hypnotic effects have tachyphylaxis-ed out, is tolerated out. The sedative effects are still there and as a result people use it for sleep. The sedative and panic attacks seem to stay on long after the hypnotic effects are gone. Now with respect to the muscle relaxing effects, I can’t speak to.
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Ritalin is a very paradoxical drug. Remember the story of how Ritalin was discovered; there was a state hospital where you had all these problem kids, conduct disordered kids. A lot of them had ADD. The director of the hospital said, “All of these kids are going to get very comprehensive medical exams.” And what he did was he gave these kids very comprehensive medical exams, including a lumbar tap. Now neurologists, tell me; what’s one of the side effects of a lumbar tap? Headache. So he was a very humane guy and he said, “These kids are getting headaches, what can we do?” Give them something to speed up their metabolism that will replace the cerebrospinal fluid and that way they won’t have the headaches. Did it work? No. But what happened was that those kids who were taking the Ritalin felt different and what happened is the teacher at the institution said, “What are you giving these kids? This is the first time these kids can actually sit in a seat and learn.” And the kids started calling them “math pills”. Why? Because they had the cognitive ability to do math suddenly? No, it was because the could suddenly concentrate for the first time. Paradoxical discovery. Remember, some things work different in kids. Barbiturates is another classic example. You give those to an adult and you are like, snoring. You give it to a kid and they are bouncing off the ceiling. Same thing with diphenhydramine, Benadryl. Some of you parents have probably seen that in your own kid, the paradoxical reaction.
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Other antidepressants: venlafaxine, that’s canadian Effexor. It works on serotonin and/or epinephrine. Relatively smaller risk of drug interactions than with some other agents. Also good for geriatric patients, in my opinion. There’s an XR form now. There is risk of elevated blood pressure. That’s maybe your one Board question, if I thought there was going to be one, is that it can – in some people – increase blood pressure. But I don’t think that’s at all a major impediment to prescribing it. Bupropion: may involve dopamine as a mechanism of action. But it’s still unclear. Low on the sexual side effects. The people who advertise it really beat that drum hard you know, and say, “Look, we don’t have the sexual side effects the other drugs do.” Possibly – this is controversial – but possibly lower induction of mania for bipolar patients. Put a check mark by there and put this, if they say, “Look, I’ve got somebody with bipolar disorder and I’m afraid to give them an antidepressant because it might send them off into mania – they are bipolar depressed right now, they are in the depressed phase – what drug do I give them?” a lot of people, the first line is Wellbutrin or bupropion. Really the ideal is lithium. Lithium is a true mood stabilizer. If you are up it brings you down, if you are down it brings you up. But it’s not a great antidepressant. It’s a mild to moderate antidepressant but it’s not a wonderful antidepressant. So most people with bipolar disorder cannot get by with lithium alone. They need lithium, for example, and another antidepressant added on to that. Your first line choice is commonly Wellbutrin, or bupropion. May cause seizure risk in bulimic patients or epileptics, important to know.
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Nefazodone, or Serzone: low sexual side effects. It can raise levels of alprazolam or triazolam, that’s Xanax and Halcion. I would put a check mark by the next one because that could be a legitimate Board question, contraindicated with these three drugs, terfenadine, astemizole and cisapride. I think that’s Seldane, Hismanal, and I think Propulsid. Trazodone, used more as a sleep agent in recent years because of sedating side effects. You know a lot of times you use trazodone at night can cause hypotension, can cause priapism. That can show up on Boards. Mirtazapine is Remeron. Pretty new. I don’t think it’s classic enough that you could see Board questions about it but, you never know. May cause weight gain, rare cases of blood problems, dyscrasia’s.

Trovafloxacin (Trovan) was a remarkable new drug and was marketed just about 1-1/2 years ago. It looked very safe and extremely effective. It was the first quinolone with very broad-spectrum activity, even against anaerobes. It seemed to be perfectly safe, very very non-toxic, until it got out into the population and there were millions and millions of doses given. With that, hepatotoxicity began to be seen and there were deaths and patients who required liver transplantation, so the drug is now restricted to very special categories. We will talk about that when we get to it. It just makes the point that with any new drug, you never really know what the toxicities are going to be – it may look perfectly safe and then you can have a thalidomide-type situation where little children are born with phocomelia – with very short arms or no arms – when there is enough of it out there and enough people have taken it over a long enough period of time. That is what happened with trovafloxacin. And then there is cartilage toxicity that is possible in children; it is really quite rare and is totally reversible, but if you give quinolones to very young puppies, usually beagles and occasionally other species, you can have cartilage deformation which, when the drug is stopped, straightens out. This is one of the reasons why these drugs have not been approved for use in children, even though they have been used widely in children.
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I have tried to summarize some of the strengths and weaknesses of the different quinolones in terms of their activity against gram-negative aerobic bacilli, pseudomonas, gram-positive cocci and anaerobes. The older ones – norfloxacin, ciprofloxacin, lomefloxacin, ofloxacin, levofloxacin – have excellent activity against gram-negative enteric bacilli. Ciprofloxacin works for pseudomonas. Against gram-positive cocci, the earlier ones have very little activity, although ciprofloxacin was approved for use against pneumococcal infections, but it is really not a very good drug for pneumococci – they are not very sensitive, nor are staphylococci. Ofloxacin and levofloxacin have better activity against gram-positive cocci than the others. None of these have any activity against anaerobes.
The trade names are as follows: Ciprofloxacin is Cipro online; Lomefloxacin is Maxaquin; Enoxacin is Penetrex; Ofloxacin is Floxin; and Levofloxacin and Levaquin. Some of the newer quinolones – sparfloxacin, grepafloxacin, trovafloxacin – are Zagam, Raxar and Trovan. Now you can virtually forget about these three, because I have already told you about the experience with trovafloxacin, so that people really are pretty much afraid to use it. Grepafloxacin has been withdrawn from the United States market because of the QT interval problem. And sparfloxacin has not been withdrawn, but it is rapidly becoming not available because of the QT problem. So these three of the newer ones are not being used or will rarely be used. They have the same excellent activity against gram-negative bacilli, poor activity against pseudomonas and only ciprofloxacin, of all the fluoroquinolones, has good activity against pseudomonas. Trovafloxacin had excellent activity against anaerobes, but the others really did not.