It is common knowledge that many typical antipsychotic agents can cause blurred vision; this is likely due to the anticholinergic activity that many of them possess. However, I recently had a patient that seemed to get blurred vision from taking moderates doses of ziprasidone. The blurred vision resolved after ziprasidone was discontinued. Ziprasidone is said to have very little anticholinergic activity. However, visual changes are listed as a relatively common side effect (3-6%). It seems unclear to me if this is still related to anticholinergic activity.

The use of valproic acid with other antiepileptic medications can also cause a decrease in the level of valproic acid itself because enzyme-inducing antiepileptic medications, such as carbamazepine, phenytoin, phenobarbital, and primidone, will increase the metabolism of valproate.

Principles and Practice of Psychopharmacotherapy, 4th Edition.
By Philip G. Janicak, John M. Davis, Sheldon H. Preskorn, Frank J. Ayd, Mani N. Pavuluri

Book Cover

The chapters are laid out in a reader-friendly manner, rather than being packed full with minutiae in a disorganized fashion. After reading this text, most people should have a fairly comprehensive understanding of how to approach the pharmacologic treatment of the major mental illnesses.

About this text, one of my mentors, S. Hinds, M.D., writes in his book recommendation list:
“Written by acknowledged giants in psychopharmacology, it is pretty comprehensive in that it spends time on the diagnosis and etiology of each disorder before launching into pharmacological treatment. It also is comprehensive about all the clinical trials used for each drug and the bottom line regarding results. I also like that they’ve expanded sections on special populations (e.g., pregnancy). So, it is the go-to source for what works and what doesn’t and the evidence for each. It is so-so regarding the mechanism of action of pharmacological agents, and, lastly, it wouldn’t kill them to just step up and give their anecdotal opinions about treatment and treatment-resistance.”

I highly recommend it.

Since lithium is a salt (lithium chloride) closely related to sodium, the kidneys will treat them in a similar fashion. If a person is dehydrated, the kidneys will try to retain salt in order to increase total body fluid volume. Therefore, until that fluid volume is replenished, excess salt will be resorbed and an increase in the levels of sodium and lithium can occur.  Significant dehydration (such as can occur with vomiting and/or diarrhea) can potentially lead to lithium toxicity.  Unfortunately, lithium toxicity can lead to nausea and diarrhea, resulting in further dehydration.

Lithium can also compete with sodium for resorption by the renal tubules and potentially lower the level of sodium in a person’s body. Those taking lithium need to maintain a regular diet with adequate salt intake and hydration.

 Partial References:
HealthyPlace.com
Bipolar World

Although it has relatively mild binding affinities for dopamine and norepinephrine reuptake pumps (at usually prescribed doses), bupropion is postulated to have its antidepressant effect through the antagonism of these pumps. Binding at other sites is even lower. Bupropion’s side effects of tremors and sweating are consistent with increased levels of dopamine and norepinephrine.

It appears, therefore, that bupropion’s metabolites play a role in its pharmacologic activity. Bupropion has several active metabolites, and their clearance is slower. The total concentration of bupropion with its metabolites likely accounts for the overall effect of increasing dopamine and norepinephrine.

With information from: Bupropion: What Mechanism of Action? Sheldon H Preskorn, MD. Journal of Practical Psychiatry and Behavioral Health, January 2000, 272-276.

Mirtazapine’s likely antidepressant action is due to antagonism of the presynaptic alpha-2 adrenergic receptors. This should allow for the greater release of serotonin and norepinephrine.

However, mirtazapine’s most potent activity is antagonism of histamine-1 receptors (thus, the sedation). At higher doses, mirtazapine also blocks 5HT2A, 5-HT2C, and 5-HT3 receptors. Antagonism of alpha-2 receptors actually comes last with increasing dosage.

Interestingly, agonism of 5-HT2A, 5-HT2C, and 5-HT3 receptors may be related to the adverse effects of SSRIs: sleep disturbance (5-HT2A), anxiety and weight gain (5-HT2C), and nausea/loose stools/vomiting (5-HT3). Therefore, the antagonist effects of mirtazapine at these sites may mitigate some of the adverse effects of the SSRIs.

With information from: Imipramine, Mirtazapine, and Nefazodone: Multiple Targets. Sheldon H Preskorn, MD. Journal of Practical Psychiatry and Behavioral Health, March 2000, 97-102.