A Few More Threads Come Together…

So…  in previous posts I’ve written about my ideas relating to blood flow and mental illness; how vasoconstriction may induce depression, and vasodilation may induce mania etc…

I wondered what would happen if someone without depression, but with schizophrenia, would take something like L-arginine (a precursor to NO, essentially a vasodilator), and those circumstances came up by chance. Sure enough, the person concerned experienced a period of mania (although described as quite enjoyable) whilst taking L-arginine for a few days.

I was thinking about this as I tried to drift off to sleep, as usual, and suddenly something which had never quite made sense started to make sense.

I could never understand why, for example, children with ADHD were given stimulants like Ritalin. You’d expect amphetamine type stimulants to make hyperactive children even more hyper, wouldn’t you? So I wondered if the mechanism which induced mania (dilation of the blood vessels in the brain causing increased blood flow and “switiching on” large areas of the brain) was the same as that which causes hyperactivity. If so, an amphetamine type stimulant causing vasoconstriction kind of makes sense in calming down this behaviour.

This got me thinking about the dopamine hypothesis of schizophrenia and psychosis. This is where you may need to take a bit of a leap of faith, but humour me for a while, hehe…

Imagine that the effects seen in some drug users which may mimic some symptoms of mental illness such as mania, insomnia etc (I’ll come to the symptoms similar to the positive symptoms of schizophrenia later) are not due to the acute effect of the substance, but a reaction to those acute effects wearing off. Imagine that when a stimulant has been taken, the blood vessels constrict, and the heart has to beat harder and faster to pump blood through these narrowed vessels, but once the vasoconstrictive effects wear off (at least, in the brain; I’m not assuming that the effects on the circulatory system are uniform and systemic) and the blood vessels relax again, the heart is still working hard, and the increased pressure forces more blood into deep structures in the brain, “switching on” parts that would perhaps lay dormant whilst the person is in a relaxed and non-threatened state. Could this be similar to the mechanism which I suggest is involved in   mania (and the fluctuations, as I’ve written in previous posts, responsible for alterations in perception and thought disturbance)?

I dunno…   there are many flaws to the dopamine hypothesis, and drugs which antagonize dopamine receptors don’t seem to have the uniform effects which you’d expect if it were correct.

I think there’s something in this, but I need to think about it a bit more.

 

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~ by funnyinthehead on November 25, 2011.

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