I respond REALLY well to clonidine, I'm on no APs, but it still works great, I think of it kinda like an earth wire for my CNS. Helps it not get shell-shocked. Human circuit breakers. Another good one is tizanidine, shorter acting, but more powerfully relaxing. And it works against tic-like clonus type stuff of non-epileptiform origins too. Its stronger a myorelaxer than clonidine, although when first getting used to it it can put you out like a light at high doses. I need it as a myorelaxer due to the spasticity in my iffy leg's calf muscle due to some neuropathy there. And whilst it isn't available here, guanfacine is used for AD(H)D and its another one of these alpha-2 agonists/imidazoline receptor ligand combinations like clonidine with a long half life. Probably makes anything like that (pretty feckin iffy) combination of amphetamines and moclobemide less prone to being quite such an insane combination too due to the way it stamps on the noradrenergic brakes.
It (guanfacine) seemingly is more subtype selective in a nootropic way.
As for the biphasic effects on concentration/attention facilitation in ADxD conditions, as I understand it, its a matter of reaching a point where the initial effect, feedback to presynaptic autoreceptors (autoreceptors affect the cellular synaptic pairing the autoreceptor is located on, whilst a heteroreceptor can affect other cells, and USUALLY although not always [an exception being the short isoform of D2, the dopaminergic autoreceptor, which is coupled to TAAR1, trace amine-associated receptor type 1, which is coupled to DAT in a negatively regulatory manner. Activation of D2Sh (there are two isoforms, D2Sh and D2-long, D2short is the autoreceptor, and reading recently allowed me to understand why D2 antagonists didn't increase dopaminergic release, and antipsychotics were antidopaminergic instead of pro-dopaminergic. The D2Sh being coupled to TAAR1, leads to on activation by an agonist, activation of TAAR1 which controls opening and closing of dopamine transporters, when activated, resulted in DAT being deactivated and thus increasing synaptic dopamine concentrations)
Theres a balance, in the case of alpha2 noradrenergic autoreceptor agonists between depression of adrenergic firing, and a sedative effect, and after a little further effect of this kind, a compensatory increase in noradrenaline is initiated IIRC, theres an overall calming and attention focusing effect, but takes kind of a hill-shaped profile, with a sweet-spot, if that makes sense between depression of noradrenergic signalling, and arousal (by this I don't mean emotional depression, but reduction in neurotransmission due to decreased noradrenaline release, and this having a damping effect on hyperarousal which itself can throw one off track, without at the same time having the dose TOO large, which causes quite a strong sedative effect. Also, for those with very low blood pressure (enough to be a clinically significant problem that is) would want to avoid it, since both the alpha2 adrenergic autoreceptor agonism, and, with these clonidine and related drugs, they interact with imidazoline receptors which also produces a hypotensive effect. Ren-since your asthmatic, do check with your doctor and make sure he knows about the asthma and its degree, since adrenaline is a bronchodilator, and so are reliever inhalers, although clonidine decreases noradrenaline/adrenaline release it does not produce a direct blockade of the beta-type adrenoreceptors, and relievers such as salbutamol (aka albuterol) and the like are directly stimulatory of beta type adrenoreceptors and themselves bronchodilatory without having to be in the presence of prior adrenergic stimulation of bronchodilatory adrenoreceptors in order to exert their effect.
Primary side effects with clonidine are in getting used to it, one rapidly becomes able to tolerate it if there are side effects, same with tizanidine (a similar drug, I take both, so am in a fairly good position to answer any 'what is it like' kind of questions. I have never taken guanfacine however, or lofexidine two similar drugs. Tizanidine is more short acting, than clonidine, but much more 'in your face' with higher doses getting used to it. First time I ever took the higher dose pills I found myself nodding in and out of sleep, with my head falling to my chest as if on opiates nodding out. Non-addictive, but if taken longterm and abruptly discontinued in high enough doses then they can cause a rebound physical effect of jitteriness, anxiety, shaky hands and increased blood pressure due to increased noradrenaline release. I have experienced that, after my psycho bitch former housemate stole and hid my meds (borderline fucking freak psychobitch from hell she was, a control-hungry power-game-playing poster child for postnatal abortion via dr.martens clinic (I.e a boot to stamp on her head as a newborn would have been a good thing for the world
) and the rebound, since I was taking a high dose of tizanidine, along with moderate clonidine dose, (near the most prescribable here for the tizanidine according to GP guidelines) it was fucking nasty the rebound. Completely lacking psychological addictive nature of any kind. And lacking psychotic hell-born whorefiends to cause such trouble, there should be no reason for such to happen in the first place.
All in all, my experience with both/either has been very positive. And damn good at overload-proofing, or at least serving as some pharmacological body-armor against autie/aspie type overloading. The only other, psycho borderline toxic hellbitch-independent side effect I myself ever get is with really high doses, which can cause orthostatic hypotension, low blood pressure upon suddenly rising too quickly from a recumbent position to an upright stance. This causes blood pressure to drop due to vasodilatation induced by the alpha2 agonist drug/s that takes a moment for the body to sense this and for a compensatory response. The way to react to this, which is easily recognizable in that it produces dizziness, in strongly pronounced cases, clouding of vision, and a ringing sound in the ears, is to hold on to something or lean against something, and to bend at the waist, so the heart has to work less hard to send blood round the body, and to rise from this position when the side effect eases off at a slower rate so the body can compensate more smoothly for it.
With a really large dose, or overdose, its quite capable of putting you flat on your back due to profound hypotension.
Do check, ren, about asthma with this drug. I would hope for it not to be much of an issue, but talk with your doctor about this, and ideally if you start, start low and work up as suits you and as needed if needed. Its always possible to put more of a drug IN to the body, far more difficult to take it out once it is in there or have to counteract it. Ephedrine or pseudoephedrine, if you really need to, induce noradrenaline release systemically in the periphery (I.e outside the blood-brain barrier) if you must counteract the effects of the drug then and there.
Also nasal congestion can be a side effect. Xylometazoline or oxymetazoline nasal drops or ephedrine nasal drops work best, I prefer the former two, and get it on a script since I take high doses of the tizanidine alongside clonidine the congestion can be really annoying with being on a lot of the two, so I get an otrivine nasal spray/drops a week, and if it gets bothersome a drop or two up the nose clears it right up, counteracting this localized effect with a localized, nonsystemic response that is completely effective in remedying any such congestion. One or two squirts up each nostril and it clears up in a minute or two at most.
