Buspar

[hry33]

this med is a tranquilliser that was heavily advertised to docs as the non addictive alternative to valium
however its generally accepted that most anxiety and panic attack sufferers dont become addicted to valium or similar meds, in fact the problem is often getting them to take a high enough dose.
buspar is often expensive and unlike valium cant be taken only as needed, it must be taken daily and wont become effective for about 7 days.

buspar is not effective against panic attacks

psychiatrists who specialise in treating anxiety and panic attacks do not use or recommend buspar.

it seems buspar is now being advertised to docs as a treatment for anxiety along with an antidepressant med as this combo is often mentioned.

some anxiety sufferers report some help from being on buspar and the side effects are generally mild

[justdontknownemore]

yeah i aggree

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[Aneri]

I generally agree with your post too. As I've mentioned in one of my other posts, I'm currently on Buspar. It seemed to have helped me with my anxiety problems, and most importantly I have not had any night time panic attacks after it kicked in (took about a week to start working).
However, I had to stop taking it in the morning because it made me very drowsy and dizzy for about 2 hours after taking it. I literally felt like one of those wild animals you see on TV after they shoot it with a tranquilliser gun (LOL). Now I take Xanax as needed during the day, and I take Buspar only before I go to bed.
Another thing I noticed about Buspar is that if I didn't fall asleep during those 2 hours after taking it, I would barely get any sleep that night. I would be mostly awake and sort of pass out for 5-15 minutes at a time (no dreams). Now, a tricky thing is that I actually fell asleep a couple of times without taking Buspar(unintentionally), so I'm starting to question why do I have to use it at all. Anyways, Buspar was prescribed to me by a regular physician, and my psychiatrist did not want to change any of my medications as long as they seem to work.
I don't think that Xanax is as addictive as the doctors claim it is.

[Just-A-Boy]

I hope this information is helpful!

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CLINICAL PHARMACOLOGY

The mechanism of action of buspirone is unknown. Buspirone differs from typical benzodiazepine anxiolytics in that it does not exert anticonvulsant or muscle relaxant effects. It also lacks the prominent sedative effect that is associated with more typical anxiolytics. In vitro preclinical studies have shown that buspirone has a high affinity for serotonin (5-HT1A) receptors. Buspirone has no significant affinity for benzodiazepine receptors and does not affect GABA binding in vitro or in vivo when tested in preclinical models.

Buspirone has moderate affinity for brain D2-dopamine receptors. Some studies do suggest that buspirone may have indirect effects on other neurotransmitter systems.

Buspirone HCl is rapidly absorbed in man and undergoes extensive first pass metabolism. In a radiolabeled study, unchanged buspirone in the plasma accounted for only about 1% of the radioactivity in the plasma. Following oral administration, plasma concentrations of unchanged buspirone are very low and variable between subjects. Peak plasma levels of 1 to 6 ng/ml have been observed 40 to 90 minutes after single oral doses of 20 mg. The single-dose bioavailability of unchanged buspirone when taken as a tablet is on the average about 90% of an equivalent dose of solution, but there is large variability.

The effects of food upon the bioavailability of buspirone HCl have been studied in eight subjects. They were given a 20-mg dose with and without food; the area under the plasma concentration-time curve (AUC) and peak plasma concentration (Cmax) of unchanged buspirone increased by 84% and 116% respectively, but the total amount of buspirone immunoreactive material did not change. This suggests that food may decrease the extent of presystemic clearance of buspirone, but the clinical significance of these findings is unknown.

A multiple-dose study conducted in 15 subjects suggests that buspirone has nonlinear pharmacokinetics. Thus, dose increases and repeated dosing may lead to somewhat higher blood levels of unchanged buspirone than would be predicted from results of single-dose studies.

In man, approximately 95% of buspirone is plasma protein bound, but other highly bound drugs, e.g., phenytoin, propranolol, and warfarin are not displaced by buspirone from plasma protein in vitro. However, in vitro binding studies wshow that buspirone does displace digoxin.

Buspirone is metabolized primarily by oxidation producing several hydroxylated derivatives and a pharmacologically active metabolite, 1-pyrimidinylpiperazine (1-PP). In animal models predictive of anxiolytic potential, 1-PP has about one quarter of the activity of buspirone, but is present in up to 20-fold greater amounts. However, this is probably not important in humans: blood samples from humans chronically exposed to buspirone HCl do not exhibit high levels of 1-PP: mean values are approximately 3 ng/ml and the highest human blood level recorded among 108 chronically dosed patients was 17 ng/ml, less than 1/200th of 1-PP levels found in animals given large doses of buspirone without signs of toxicity.

In a single-dose study using 14C-labeled buspirone, 29% to 63% of the dose was excreted in the urine within 24 hours, primarily as metabolites; fecal excretion accounted for 18% to 38% of the dose. The average elimination half-life of unchanged buspirone after single doses of 10 to 40 mg is about 2 to 3 hours.

The pharmacokinetics of buspirone HCl in patients with hepatic or renal dysfunction has not been determined, nor has the effect of age. The effect of buspirone HCl on drug metabolism or concomitant drug disposition has not been investigated.