I’ve been reasonably stable (or at least no one has complained loudly) over the past several years by taking Lamictal alone for bipolar. However, my moods have gradually gotten out of control over the past year. I realized (and admitted) that I needed a meds adjustment, so I found a psychiatrist who believes in the teamwork approach to meds management. Thus, she sent me on a quest for new medications; I’ve always been opposed to lithium, but she asked me to consider it and also to look into the anti-psychotics. In fact, she loaned me a book that describes the mechanisms behind how (it is believed that) they work. Unfortunately, I returned the book before I got this idea of sharing with you how these medications work, so I will have to rely on my own notes and conclusions.
DISCLAIMER: I am not a psychiatrist, psychologist, M.D., D.O., medical student, or even a biologist, nor do I play one on TV. I am not an expert, just an intelligent individual with an inquisitive mind. Please keep this in mind as you read this post.
The book I read is called: Psychosis and Schizophrenia: Thinking It Through. It’s published by Neuroscience Education Institute, but it was written by Stephen M. Stahl. It’s full of amusing pictures, informative descriptions, and lots of technical lingo. Now, on to what I’ve learned (or think I’ve learned):
The theory is based on the idea that dopamine plays a major role in schizophrenia. There are five basic dopamine pathways (DA) in the brain:
(1) mesolimbic pathway
(2) mesocortical pathway to DLPFC (dorolateral prefrontal cortex)
(3) mesocortical pathway to VMPFC (ventromedial prefrontal cortex)
(4) nigrostriatal pathway
(5) tuberoinfundibular pathway
I have no idea who names these things, but I think of them as a bunch of little roads that all come together in (more or less) a central location in the middle brain. Some of them are long roads and some are short roads, some work just fine (#4,5) whereas others either don’t work well enough (#2,3) or they are working overtime (#1). The consequence of this “out of tune” situation, as Stahl puts it, is delusions, cognitive impairment, and depression.
There are several main receptors involved in this dopamine dance: 5HT1A, 5HT2A, D2, D3, M1, H1, and α1. Some of these need to be increased and others decreased to bring the flow back into order. Medications act on these receptors in a variety of manners: some act as blockades, others act as agonists (stimulating the receptors) while others work as antagonists (reducing cell action), and then there are those that are partial agonists, partial antagonists or partial blockades. Many medications are combinations of these effects.
What’s this got to do with anything? It has everything to do with side effects!
As I understand it, some of these receptor sites have to be blocked in order to get the traffic flowing at the correct rate. Depending on which site you decide to block, you get a different set of side effects. For example:
M1: constipation, blurred vision, dry mouth, drowsiness
H1: drowsiness, weight gain
α1: drowsiness, low blood pressure, dizziness
Now that we have gotten through all that… let’s look at the conventional v.s. atypical anti-psychotics.
Conventional anti-psychotics create a chronic D2 blockade. What does that mean? Normally your neurotransmitters latch on to a receptor site and pass the signals along, however, a D2 blockade cuts in and blocks the neurotransmitter from reaching the receptor. If we go back to our dancing analogy, it stole your dance partner and won’t give him or her back!
Atypical anti-psychotics only borrow the receptor sites. So it’s more like square dancing; the medicine cuts in, twirls about for a bit, then wanders off letting things go back to normal. This interruption process provides a better “traffic flow”. Most of the atypical anti-psychotics appeal to a variety of receptor sites, which creates a mixture of side effects.
Basically, it’s all a dance: activate this, deactivate that, fully or partially blocking, all in an effort to regulate the “traffic flow” of dopamine and serotonin.
That’s how it works for schizophrenia. Why do the same medications work for bipolar? Well, the experts are still working on that.
(Note: The University of Utah has a very nice website that discusses neurotransmitters and pathways with respect to addiction. It is a great resource for understanding the principles of reward pathways in the brain.)
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