On 30 Oct 1995 08:31:07 -0800,
Jason Kennerly <jkenner at cello.gina.calstate.edu > wrote:
>Sandra L Wegert <sandraw at U.Arizona.EDU> writes:
>> On 27 Oct 1995, Jason Kennerly wrote:
>> I was under the impression that ADD involved a sort of depression; people
>> with this problem are trying to stimulate themselves behaviorally in
>> order to distract themselves. What stimulants do then is take over the
>> job, so that the person can give attention to other tasks. By the way,
>> several GRAMS of caffeine can be taken, with uunpleasant side effects,
>> but no actual danger (except in a very few individuals).
>>The "sort of depression" involves impulse regulation centers of the
>brain, which dopaminergic stimulants act on almost directly. Caffeine, on
>the other hand, is what I affectionatly call a "full-brain" stimulant, or
>what the doc's call a cellular stimulant... and as such caffeine will
>stimulate ANYONE except caffeine users in withdrawl.
>
Usually when people talk about something like the coexistence of ADD
and depression they are referring to depression as a clinical
diagnosis. How much this helps in the clinical management can be
open to question - it often leads to an ever escalating pattern of
medications and side effects.
What this points up is one of the fundamental problems of psychiatry
- there isn't a very good correspondence between pathophysiology and
clinical presentation. There have been anecdotal reports of improved
clincial management through the use of functional imaging techniques
such as SPECT. Whether functional MRI can perform the same task has
not been researched to my knowledge.
There is another aspect though to the comorbidity of ADD and
depression which I think is quite interesting, and has to do with
an expanded definition of the term "depression" and the concept
of a broad spectrum of functional brain disorders, which
includes many of the psychiatric disorders and the so called
"psychosomatic" disorders, and possibly even the autoimmune disorders.
In fact, physicians often use the term "depression" in this extended
sense when they inform patients that their physical symptoms are the
result of "depression", even though there may be only minor
disturbance of mood or affect. This alternative use has been a great
source of confusion and misunderstanding, and has been bitterly
resented by many patients.
"Depression" is really a very loose term, like "cancer". In the same
way that a leukemia is very different from breast cancer, the
"depression" of CFS or substance abuse is quite different from Major
Depressive Disorder. Now that the pathophysiology of many of these
disorders is finally beginning to be understood, a new terminology
seems to be in order. In any case it is about time that psychiatry
abandoned the use of familiar English terms for medical conditions, to
bring it into line with the rest of medicine.
Various lines of research seem to point to two major classes of
depression, possibly related to brain dopaminergic (catecholamine) and
serotonergic (indoleamine) pathways. The extensive interactions
between these pathways complicates the picture, because the
therapeutic actions of psychotropic medications are often not fully
explainable in terms of their immediate receptor action - Prozac is a
good example.
In the extended sense, ADD itself could be regarded as a form of
"depression", requiring boosting of brain catecholamines.
AJR
