Click here to view next page of this article

 

Clinical Aspects of Depression

Women are at least twice as often get depressed as men, and even women when women are equal, which will not be in my lifetime, they will still have more depression than men. The four somatic symptoms could be any of the above, and I think that some of these everybody is going to be asking about, because most physicians would ask about weight gain, most would ask about sleep. This would come in but here are the things that might not be depresion.

Major depression, depending on what data you look at will be 2:1 or 3:1. If you look at seasonal affective disorder or seasonal depression, it’s 4:1. There is a 5% lifetime prevalence, so it’s one of the commonest diseases that we know of.

Depression has a huge rate of recurrence. It is a chronic disease so the treatment has to be modified to take that into consideration; because there was a lot of nonsense talked about it in terms of just what caused the depression and I’ll come to that in a minute.

One of the things is that there is an incredible amount of use of emergency rooms and primary care physicians. Of course psychiatrists today, as opposed to 20-years-ago mostly see depressions after they have been to other doctors.

The core morbidity problem is very interesting, because in our clinic about 60% of our patients with a diagnosis of major depression have a morbid medical illness. Seventy-percent of our patients with schizophrenia have a medical illness and we don’t include obesity and we don’t include tardive dyskinesia or addiction.

A word about medications that may be used for depression … there are really a tremendous number of them.

Differential diagnosis, this would be a tendency in the medicine, and even among certain psychiatrists, to think that if somebody has a severe trauma then you can understand that that might make them depressed. If I had a car wreck I am unlikely to be elated. On the other hand the important thing is that because you think you can understand that they might be depressed.

Secondary depression would be important because we can have various organic disorders and they cause secondary depression. One of the things that might be included is that depression can begin at any age, from the teens.

Obviously dementia is another factor one would take in consideration because in many ways some of the things that are the insidious factors in depression, for instance if somebody loses a little bit of interest and doesn’t concentrate quite as well and isn’t as energetic as they would like to be, or they might have been, if you are 30 then people get alarmed and wonder what’s going on.

The emphasis on major depression will be to make the appropriate diagnosis and to treat aggressively. This was perhaps more important in the days when people relied on tricyclics because people would say that the psycho-pharmacologist was somebody who went around and increased the dose of antidepressants and decreased the dose of antipsychotics. Because there was a tendency to underdose. With the newer SSRI’s that is less of a problem. Given that the natural history is would be true for people who had more than one episode.

In terms of the treatments that are available, there is pharmacotherapy and psychotherapy. A word about psychotherapy because much of this, the literature, has been diluted by some of the grandiose claims in the past that were unproven about psychotherapy, for whatever ails you, whether it was ulcerative colitis, or the sexual dysfunction.

You could think of it that if you got very mild depression, you get better no matter what happens.

We talked about past response, clearly if somebody responded in the past to a treatment, you are going to give it to them again. If there’s a family history of depression and they responded to brand X, then you would jump for brand X. The clinical subtype would really be that there are so-called anxious depressions, so-called atypical depressions.

So this really takes us into selecting pharmaceuticals. We’ve got trazodone here, we have nefazodone and we have venlafaxine, which is both a drug that has an effect on norepinephrine and on serotonin. As you may recall, yesteryear there was a big controversy between the London group who felt that serotonin was the thing and the Boston group who felt it was norepinephrine, and they probably are both have a little bit of the truth. In point of fact, the drugs that have both an effect on serotonin and norepinephrine may well be the most potent, albeit the more difficult to use. I think most people use trazodone as a hypnotic or as optimistic thinking that might help getting erections. Very few people I know use it as an antidepressant. Nefazodone will be used a bit more often. It’s a very sedative-type drug.

Tricyclics. The problem with them being there’s not a therapeutic window. It’s not as narrow as you would think in reading all of the recent studies. For instance, all of the new antidepressants go against imipramine and amitriptyline. Well, I don’t know any psycho-pharmacologist who has used imipramine or amitriptyline, unless there is a special reason, in years. Because the secondary means like desipramine and nortriptyline have much less sedation and much less logy feeling and are equally efficacious and are easier to monitor. So in point of fact, nortriptyline would probably be people’s drug of choice. What you have to say more is, that it’s much easier to kill yourself with tricyclics.

There’s a whole range, there’s a couple of other ones out now, but I would just mention that probably you should learn to use one of two drugs. There’s no data apart from that data to suggest that these drugs are any different.

So while we are waiting for the data, I would not have a failure on Prozac and go on to Zoloft or go on to Paxil. If I failed in one, I would jump into a different group. Probably the group that we would recommend, because you are probably familiar with it from other areas, would be a drug like bupropion. Because it has a different mode of action. It has an effect on norepinephrine, it has some slight effects on dopamine. It is getting pushed quite a lot for smoking cessation, whereas it has a definite but modest effect, and it is more of a stimulating drug than some of the others. I think if someday you felt sure of your diagnosis and you were to use the paroxetine, if you gave somebody 20 mg of paroxetine and waited a month and nothing had happened, I would double the dose and go up to 40 and wait another 2-3 weeks. If nothing had happened by then, I would change.

Drugs like venlafaxine have an effect both on serotonin and norepinephrine. It has a bit of a problem, since this is a multiple-dosing drug. These are drugs that you can give all at one time. Indeed, I have a colleague in England who used to give, when Prozac was coming out, he used to get patients in and give them the seven tablets in his office, and they never got any more Prozac until they came back the following week. So they are relatively safe drugs and of course fluoxetine is a very long-acting drug, which is both a plus and a minus. The reason why I didn’t chose sertraline, which is Zoloft, is it is a multiple dosing drug and the dose of Zoloft is probably 200 mg for a lot of patients, so you go to 100 mg and wait. But you have a decision to make about increasing the dosage. We would tend to push the dosage up to 200 mg. Similarly, if you choose Prozac, even though there are early studies showing that there’s no difference between 20, 40 and 60 mg fluorite and the latest studies from the Mass. Medical Health Center suggest that if you go up to 40 mg a day of Prozac you will get a better result.