Re: Please Help Scott

Hi Andrew.

> The friend apparently will refuse to continue Haldol because it makes him feel anxious.

It could be akathisia. However, it would be difficult to evaluate someone for this condition if the patient remains in bed, as many of the symptoms depend on observing motor activity while sitting or standing (rocking back and forth in a chair, pacing, shifting weight from one foot to the other). If the patient describes extreme restlessness, having an urge to move, and a feeling of "crawling out of their skin, akathisia is likely present. This side effect can be treated with Cogentin (benztropine), a potent anticholinergic. Ugly.

Unfortunately, anxiety (not akathisia) is a common reaction more often seen with the older neuroleptics. I think I read that trifluoperazine is the worst antipsychotic with respect to anxiogenesis. I'm not sure, though. The anxiety side effect is often treated with a benzodiazepine. Ugly.

Haldol is a heavy-duty drug. It binds to dopamine receptors with high affinity, and isn't terribly selective (D1-D4). This might be the reason why the risks of developing dystonias and tardive dyskinesia is so high. For this reason alone, I would not make Haldol the first choice for maintenance treatment.

One of the defining characteristics of atypical antipsychotics that the first generation antipsychotics lacks is their ability to block 5-HT2a receptors. This is good for anxiety.

Does your friend acknowledge that treatment with Haldol effectively mitigated his paranoid delusions? Is he willing to switch to another drug? You can explain to him the differences between Haldol and the newer atypical antipsychotics for which the risks of akathisia and anxiety are greatly reduced.

Thanks for the information regarding inflammation and curcumin. I tried minocycline. At first, it helped quite a bit. After 1.5 years, I began to develop hyperpigmentation of my feet and shins. At that point, I discontinued it. However, I did not experience a worsening of depression. Perhaps its benefits waned over time so gradually that I didn't notice it.

> Interested in the inflammatory/immune system component of BP. What do you know about that?

Gosh, that's a big subject. Microglia cells in the brain release pro-inflammatory cytokines which modulates the immune system. Evidence for the involvement of inflammation in mental illness is mostly empirical. People with mood disorders have higher levels of inflammatory markers than healthy people. The question I have is which came first, the depression or the inflammation. I think it possible that depression comes first. This might then provoke microglia to produce pro-inflammatory cytokines. I imagine arguments can be made for the reverse, though. However, Duke University found that the levels of inflammation increase with each successive depressive episode. I see this as being consistent with the first explanation. Whichever be the case, I think a positive feedback loop is set up for the perpetuation and/or worsening of the depressive state. I don't know. Maybe damaged cells resulting from glutamate excitotoxicity is the provocation for the induction of the immune system. C-reactive proteins are also elevated in depression. But I ramble. Suffice it to say that brain inflammation is associated with mood disorders.

I look at the Bipolar Network News (BNN) frequently. Here is what came up on a search:

Some see things as they are and ask why.
I dream of things that never were and ask why not.

- George Bernard Shaw

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