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  © 2008
  University of Idaho
  All rights reserved.
  Psychology Dept.
  University of Idaho
  Design - P&D  CTI

In general, mood disorders are classified into two major groups; Unipolar disorders which we usually consider depression and mania, and Bipolar disorders.  So, let’s talk about the most common disorder (on slide four), which is called unipolar depression.  Unipolar depression was first described by Hippocrates.  Basically, he thought that depression was caused by an excess of a body substance that he called black bile.  The term melancholia is basically equivalent or translated to black bile. 

While Hippocrates was wrong about the actual cause of depression, he was really the first to propose that a psychological problem could actually have a physiological cause.  Today, as we see in slide five, depression has been described in approximately 5% of the world population, and 8 million people in the United States currently suffer from this disorder.  In addition, more than 70% have more than one episode of major depression or unipolar depression.  The average age is age 28, and women tend to be affected two to three times more often than men.  However, that may be somewhat inaccurate because men, oftentimes, do not seek out treatment.  So, there may be a diagnosis issue.

In addition to that, unipolar depression occurs both in young children and in the elderly. Unfortunately, most of these individuals are not diagnosed.  Unipolar depression also has several major sub-types.  As we can see here at the bottom here (slide 5), melancholic depression, atypical depression, and dysthymia all are part of what we call the unipolar depression disorder.

Unipolar depression is categorized by several symptoms (see slide 6).  These include unpleasant moods, mental anguish, inability to experience pleasure, and even a loss of interest in the world.  However, when we look at symptoms, there are three major symptoms that are required before one can be diagnosed with unipolar depression.  These symptoms are listed on slide seven, and as you can see, there are quite a few.

In addition to those symptoms, there are a couple of other things that needs to be occurring before we can get a label, or a diagnosis of being depressed.  First of all, as we see in slide eight, the depression needs to be greater than some kind of loss that’s experienced.  That is, if you have someone that has died in your family, it would be very common to be depressed for a period of time. On the other hand, if your depression occurs because your fish died, that might be a problem.  The duration as well is important.  Usually, most people who are depressed may have symptoms that last a few days.  However, in most people with a major depressive disorder, the depressive state lasts for weeks or longer.  The lack of a precipitating event can also lead to the diagnosis of a depression.   Also, if it is not pervasive or unrelenting (basically it continues on), and there are no other health disorders involved (For example, often individuals with thyroid problems will show symptoms of depression.  However, if one examines a thyroid and does a thyroid screening exam and there are no major thyroid problems, then a diagnosis of depression may be in order).

Regardless, as we see in slide nine, the diagnosis of depression should be done by a professional, and there are many types of tests one can use for the diagnosis of depression.  The classic one comes out of Psychology and is called the Beck Depression Inventory (or what’s called the BDI).

 Now there are several subtypes of unipolar depression, and we saw that a little bit earlier in the presentation, melancholic, atypical and dysthymic.  So, let’s talk a little bit about each of these.  First, as we can see in slide 11, melancholic depression is the most frequent, and it occurs about 40 to 60% of the time.  It has no precipitating events and oftentimes occurs more than one time.  It may lead to motor retardation.  It also responds well to a variety of different treatments such as electroconvulsive therapy (which we’ll talk about a little bit more detail later), tricyclics, and SSRIs which are types of drugs. 

Atypical depression, on the other hand, is less calm than melancholic depression.  These symptoms tend to be opposite of melancholic depression.  It appears earlier, it tends to be chronic, and individuals with atypical depression can even cheer up temporarily.  Oftentimes these individuals (instead of having sleep problems or the lack of eating), tend to overeat, they sleep more, and the depression is worse in the evening.  These individuals, as we can see on the bottom of the screen, respond better to what are called MAO inhibitors (which are called MAOI’s and are a different type of drug category).  Again, we’ll talk about these in a little bit in more detail later.

Dysthymia is a milder form of depression and can last for years.  The symptoms are milder, and as a result usually do not cause as many problems. 

Well, what are some causes of depression?  Well, the first and major one (as we can see in slide 14) is from genetics.  As we can see here, concordance rates for bipolar depression can reach as much as 80% in monozygotic twins.  Suicide rates are also very high as well.  Regardless of the correlations that we have with depression, no one specific gene has been identified, although chromosome 18 has been linked with depression. 

A second major hypothesis for depression involves what is called the biogenic amine hypothesis.  This develops from the catecholamine hypothesis which is that norepinephrine, serotonin and other types of neurotransmitters cause depression.  Basically the biogenic amine hypothesis says is that depression occurs from a reduction in norepinephrine, serotonin, or both. 

There is a lot of support for this hypothesis.  As we see in slide 16, we find that if we give certain types of drugs, such as MAOIs, tricyclics, or selective serotonin reuptake inhibitors, they increase the levels of biogenic amines, and as a result, decrease depressive symptoms.  ECT also increases serotonin levels as well.  So, it’s commonly believed and hypothesized that the depression is caused from some kind of problem with these levels of neurotransmitters. 

The problem with this disorder and this hypothesis is that tricyclics and serotonin reuptake inhibitors rapidly block the reuptake systems of norepinephrine and serotonin.  However, even though the blockage is very rapid, the recovery from the depression often is very slow, and often takes weeks although some people actually have increases in serotonin levels.

Another hypothesis relates to neuroendocrine functions.  Severely depressed individuals oftentimes have decreased secretions of adrenocortotrophic hormone which is secreted by the pituitary.  As a result, it increases levels of cortisol from the adrenal cortex.  This process follows a particular circadian rhythm that we have in our body.  As we can see here in the bottom of the slide, depressive individuals also have disruptions with circadian rhythms and these return to normal levels following recovery from depression.

So as we can see, there’s a variety of different hypotheses that are out there.  But, it’s not as clear cut as it used to be, and depression may involve multiple symptoms. Regardless of the cause, however, there are very effective treatments.  So let’s talk about some of these treatments and get an idea about what they are.

The first treatment that we use for unipolar depression basically involves drugs.  As we can see here (slide 20), there are three major categories of drugs.  In addition, there is another treatment called electroconvulsive therapy which we’ll talk about in a few minutes.  So let’s talk about each of these drugs in a little bit more detail.  Tricyclic antidepressants basically block the reuptake of norepinephrine and serotonin.  So, what is happens that the neuro-transmitter is released; it binds on the receptor site.  Then normally the serotonin or the norepinephrine is reabsorbed back into the presynaptic element.  Tricyclic antidepressants block this reuptake. As a result of that, it increases the levels of these neurotransmitters.  In addition to that, it also blocks the postsynaptic histamine receptors and postsynaptic acetylcholine receptors. 

There are many types (as we see on slide 22) of tricyclics.  Probably the ones that we hear about most of all are amitriptyline or elavil, and impramine which is called trofranil that’s out there on the market.  But, there are many, many other types listed as well. 

There’s a wide variety of clinical limitations to the tricyclic drugs.  First of all, they have a slow onset of action, oftentimes four to six weeks.  They exert a wide variety of effects on the central nervous system, and they cause a wide variety of side effects that are not shared by a number of other medications such as the SSRIs.  In addition to that, tricyclics can be cardiotoxic and thus can cause you to die if you are not monitored adequately. 

The one advantage about tricyclics (as we see in slide 24) is that they don’t produce euphoria in normal individuals.  Thus, they’re not reinforcing and you have low abuse problems.  In addition to that, there are usually no problems with withdrawal.  They also have a long half-life, so they’ll stay in the body for a longer period of time.  They also readily cross the placental barrier, and so they can be passed on into newborns.  That’s a potential problem with some compounds.

Well, that’s the first type of drug that is used to treat depression.  Now, there are other types of drugs as well.  The next category of drugs is called monoamine oxidase inhibitors, or what are called MAOIs.  Monoamine oxidase are enzymes and they break down norepinephrine and serotonin after they’re released.  There are two different types of monoamine oxidase, and they have kind of been labeled A and B or good and bad depending upon where they’re located.  Monoamine  oxidase A is basically responsible for the blockage and occurs with antidepressants, and B is responsible for the side effects that we have.  So by blocking monoamine oxidase A, you increase the person’s mood and you decrease the depression.  Monoamine oxidase B basically causes lots of the side effects which we’ll talk about soon.

Now related to monoamine oxidase are what we call the monoamine oxidase inhibitors. These have been around for quite a period of time, have some very serious side effects, and you have to be careful with them.  They can be as safe as TCAs or SSRIs (which we’ll talk about in a few minutes), they tend to work on patients who don’t respond well to other drugs, and they are also excellent for atypical types of depression.

As we see in slide 28, there are a variety of different types Phenelzine is the classic one and Marplan is one that’s used often as well.  Both of these particular drugs (and others) block both types of monoamine oxidase.  So, they’re going to inhibit the secretion of both types of monoamine oxidase.  As a result of that, you increase your levels of norepinephrine, serotonin, and also dopamine within the synaptic cleft.  Thus, you have more firings on the next neuron and you don’t become depressed any more. 

However, as we’ve talked a little bit about, there are a wide variety of side effects which can be fatal.  As we see in slide 29, there are a variety of different things you have to be careful of.  Particular types of fermented foods can cause major problems including cheese, beer and other things.  In addition to that, other, some particular types of medicines such as nasal sprays and other cold medications can cause major problems, and even result in death. However, as we see in slide 30, MAOIs can be extremely effective if used carefully and a lot of people use them for particular types of depression. 

The next category of drugs that I want to discuss are called serotonin specific reuptake inhibitors or what we call SSRIs.  What these drugs do is block the reuptake of serotonin from the synaptic cleft.  They basically work the same way as the tricyclics do, it’s just that the target neurotransmitter is serotonin rather than norepinephrine.  However, they don’t block other neurotransmitters.  In addition, all appear to be equally effective but they’re not interchangeable.  In addition to that, SSRIs have been used for a wide variety of other disorders such as bulimia and ADHD as well.  There are a wide variety (as we see on slide 32), of side effects that are associated with SSRIs.  For example, you can get confusion, fevers and chills, agitation, etc. However, this usually occurs in combination with some kind of other drug that the person is taking.  The key thing is that 60% of the individuals develop some kind of serotonin withdrawal syndrome when they stop taking SSRIs.  That can cause some major problems when bringing being the person off the particular drugs.

There’s a wide variety of different types of SSRIs and I’ve listed several of these on slide 33.  The one that you probably often hear about is Prozac or Zoloft, but there’s a wide variety of other ones as well.  The problem with SSRIs is that often times when we give them in double bind studies they have the same effectiveness as a placebo.  That’s a problem with a lot of depressive agents as well. 

Well we’ve talked about a wide variety of drug treatments for depression.  What about some other types of treatments?  The other type of treatment that we really talk about with depression today is what is called electroconvulsive therapy.  ECT can be extremely useful in the treatment of depression, especially major depression and oftentimes will produce full remission or marked improvement in over 85% of the patients who have major depression.  That means that these people do not have depressive symptoms any more, nor do they show relapse of the symptoms.  The ECT today is not the same that we used to see in the old days (such as the 1920, 30s, and 40s) or where we watched One Flew Over the Cuckoo’s Nest (which had major, major problems).  However, the treatment is much more effective and humane today although it still causes a brain seizure.

  In general, what we usually use is about six to eight treatments of ECT for depression today.  Usually what you end up with is complete remission of all the symptoms of the depression.  Why?   We have no clue.  A lot of people hypothesize that you get increases of serotonin and that’s what causes the recovery.  However, the reason for its effectiveness is still unknown.  You still may get some memory loss from ECT but it is usually short term and usually is recovered over time as the procedure continues.

Well we’ve now talked about a wide variety of different types of unipolar depression.  There’s another type of unipolar disorder as well.  That is mania.  Mania is a little bit different than general hyperactivity that we normally see with a lot of people.  As we see in slide 36, persons with mania are literally bouncing off the walls.  The person, talks real fast, has major confusion; they go from one topic, to another topic, to another with no closure on anything. In essence, the person becomes, as they say, extremely, extremely manic.  The treatment for mania (as we also see in slide 36) is what are called lithium salts. What these treatments do is stop the manic episodes.  However, lithium is also extremely toxic to the liver.  Thus, good follow-up measures need to be put in place.  Often people who are on particular types of lithium medications have monthly or bi-monthly examinations for liver functioning. 

Well we’ve talked now about two major unipolar disorders, what are the other major types of mood disorder.  One is called bipolar disorder.  Here, what we have is an alternation of mania and depression.  Usually it occurs following some particular type of depressive episode.  Oftentimes the person goes in cycles.  You might see a seven or an eight month cycle where a person will go from mania, into kind of being relatively normal, to being severely depressed, back to somewhat normal, and back to being manic again.  In essence, it may take several weeks before the particular drug becomes effective treating the disorder.  Oftentimes individuals will check themselves into hospitals when they know they’re getting severely depressed or severely manic. 

The last major type of disorder that I wanta talk about is what we call seasonal affective disorder.  Usually this is the form of depression.  Often  we see this disorder in the winter months.  Nobody really knows why it occurs, although some individual hypothesize it occurs due to visual stimulation within the cortex.   What seasonal affective disorder involves is mood and sleep disturbances.  Often  you see carbohydrate cravings and you may see major weight gain.  The classic treatment for seasonal affective disorder is phototherapy.  That is, you get a person and you expose them to bright light for certain periods of time.  This helps improve their mood.

In general, depressive disorders, although they’re a wide variety of different types, can be effectively treated, and when they are treated, the person can function relatively normally.

In our next section, we continue on talking about major disorders and we’re going to talk about a specific type of memory disorder, that is, Alzheimer’s disease, so until then we hope that you are having a great day.