rakketakke
Bluelighter
SSRI's, SNRI's and i believe most tricyclics and MAOI's are also not recommended for anyone under 18. Doesn't mean it's poison though. Seroquel has not decreased my ability to learn, nor has my muscle tone decreased, nor have i gained weight nor have i developed diabetes. It doesn't make you think less either it just acts as a antagonist at certain serotonin and dopamine receptors hence it's anti-psychotic effects. The severe drowsiness caused by seroquel is due to it's H1 antagonism and also it's anti-Adrenic effects. When you get into the higher doses as in 200mg's+ a day then it starts to antagonize certain serotonin subreceptors and if you get to a high enough dose dopamine receptors too mostly D2.
The trials you are talking about to see if seroquel, zyprexa and i believe risperdal worked better then typicals are kinda iffy. I think zyprexa was the most tolerable of the lot. Atypicals tend to work better on the negative symptoms or atleast i believe seroquel and a few others do. I have had the typical anti-psychotics Thorazine and methotrimeprazine. Thorazine was actually quite tolerable even at 100mg's and it sure stopped my puking rather well. I didn't even find it as sedating as seroquel. Methotrimeprazine is a rather week anti-psychotic but due to it's rather potent anti-histamine and anti-cholinergic effects it's so sedating it makes both seroquel and Thorazine look like Amphetamines by comparison.
Once i got used to seroquel i noticed no dulling effect and in fact it stopped my brain from overreving so that i could fucking think. Zyprexa works much better for me but i can't afford the shit. I'll take the risks of seroquel any fucking day over existing in a manic depressive hell.
I suppose you're lucky, i've had it all from seroquel/risperdal. Not something to take for insomnia, i'd rather not sleep and still have sex.
"Neuroleptics (a broad category of antipsychotic drugs) were discovered by accident in the 1950s when Henri Laborit administered chlorpromazine, for its antihistamine effect, to patients being prepared for major surgery (Laborit & Huguenard, 1951). He observed that the chlorpromazine provoked mental effects such as decreased interest in the environment. This observation encouraged his colleague Jean Delay to test the action of this drug for antipsychotic potential (Delay, Deniker & Harl, 1952).
Chlorpromazine opened the door to the production of many other drugs with antipsychotic effects. (Table 1 lists the most widely used antipsychotics in Europe and the United States and their effect on sexual response.) Soon afterward, it was found that chlorpromazine— and, somewhat later, that other antipsychotics—had signifi cant undesirable side effects on motor and muscular activity, inducing parkinsonism (Parkinson’s-like symptoms) and tardive dyskinesia (late-developing movement disorders). The muscle stiffness and uncoordination or lack of movement produced by these drugs was referred to as neurolepsis, and the term neuroleptic was coined by Laborit and Huguenard (1951) for the antipsychotic drugs that produce the undesirable motor effects. The effects were shown to be produced by the blockage of D2 receptors in the striatum (a subcortical region of the brain containing the putamen and caudate nucleus), which controls motor activity (D. Hartman, Monsma & Civelli, 1996; Jentsch & Roth, 2000). The striatum is a component of the extrapyramidal motor system (as distinct from the pyramidal, or corticospinal, motor system that originates in the motor cortex). The striatum receives dopaminergic fibers via the nigrostriatal pathway, which consists of axons originating in neurons located in the midbrain substantia nigra (Bjorklund & Lindvall, 1984).
Patients treated with antipsychotics frequently reported sexual disorders, though initially they were not taken seriously. Men frequently complained of erectile and ejaculatory problems. For example, in one study, half of the patients receiving thioridazine (Mellaril) reported disturbances in ejaculation (Kotin et al., 1976). Some of these sexual effects, such as erectile disorder, are not due to the effect of these drugs on the striatum or on dopamine receptors. Instead, they are due to the blockage of muscarinic cholinergic (acetylcholine) and alpha-adrenergic (norepinephrine) receptors in the peripheral nervous system or spinal cord that are related to erection and seminal emission. Anorgasmia and alterations in libido and sexual gratifi cation were also found in men and women treated with neuroleptics (Ghadirian, Chouinard & Annable, 1982; Shen & Sata, 1990). Adverse effects on orgasm have been observed with both lowpotency neuroleptics (i.e., those having little effect on cholinergic receptors), such as chlorpromazine and thioridazine, and high-potency antipsychotics (having strong effects on cholinergic receptors), such as fl uphenazine and haloperidol. Anorgasmia caused by antipsychotics is apparently due to their effect not on the striatum but rather on the limbic cortex, a separate region to which dopaminergic neurons project (Bjorklund & Lindvall, 1984). The cell bodies of dopaminergic neurons that project to the limbic cortex are located in a different part of the midbrain (not the substantia nigra), in a region termed the “ventral tegmental area.” Their axons form the mesolimbic dopaminergic pathway."
So yes, seroquel is a new generation but I completely understand the poison argument. Still a long, long way to go.
Great basis!
My whole life I could read 1000+ pages in 1-2 hours without losing focus, when taking Risperdal and a very, very long time afterwards I had troubles comprehending what I was reading. Sometimes even reading a line and it wouldn't even enter my brain. The cottonmouth was also ridiculous.
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