Occasional Use of Ambien

In My Humble Opinion
1

For many years now I have made occasional use of Ambien to get a good night’s sleep. I would use it no more than once a week, usually less. It seemed to work fine and did not seem to interfere with getting to sleep on those nights when I did not use it. About two years ago I went through a period of about two months where I used it every day. I weaned myself off it (going sleepless for close to a week) and returned to my poor, but reasonably stable sleeping habits. However, I seem to have lost my ability to use Ambien occasionally. Now when I use it (and I rarely use it more than once a month), it generally means that the next night I sleep very little.

Having written this, I can see that I have answered my own question, which was “Have I been sensitized to Ambien so that dependency kicks in immediately?”. Obviously, I have. I would still like to hear other people’s experiences.

2

Ambien is not a benzodiazepine, but I’ve been told (by a real live Medical Doctor) that it operates in much the same way as benzos do.

Based on my experience with one particular benzo (clonazepam, a.k.a. Klonopin), I’d be very afraid to use Ambien they way OP describes, fearing exactly the same result OP describes.

I can’t be sure how relevant my experience is, but that’s the input I am able to offer in this thread.

3

I think it varies greatly on the individual. I don’t have an addictive tendency at all. Luckily.

I’ve taken different sleep aids, tranquilizers and anti-anxiety meds over the years trying to find what’s perfect for me. I zonk out for days if I take a normal dose of most of them, even over the counter stuff like melatonin and valerian. So now I take Sonata which only lasts about 4 hours in most people. It’s great because by the time you realize you have insomnia, it’s already 2am. And I also am on clonazapam as needed and it works well for me. I have no residual deprivation in the days following.

It could be that you’re just so well rested from night 1 that you don’t need as much sleep on night 2. That happens to me occasionally, whether I’ve medicated or not.

But whatever the theory, definitely tell your doc. There are lots of alternatives. My hubby swears by melatonin. I hate it.

4

I also use ambien now & then - times when I have started using it frequently I find it doesn’t work nearly as well.

now, I save it for travel or other times when I know sleeping will be a problem.

long term, it’s really worth working on relaxation in general: stress reduction, sleep “hygiene” issue (have you tried a sleep mask?) all of it. try yoga, seriously.

5

Some people can be unusually sensitive to rebound insomnia. About 12 years back, I did a trial of 2 weeks on Ambien, then stop it and have it around to take on occasion if I was really having trouble with my Restless Legs Syndrome. This was because I did not, at that point, want to go on one of the dopamine agonists which are standard medication for the condition.

The first night or so after the 2 weeks was bad. I stubborned it out, but after that if I felt the need to take Ambien, I had to weigh it against the fact that the next night I’d be in hell. So I either did without, or planned on taking it for the rest of that work week so I could be brain dead on the weekend.

At least one doctor expressed surprise that I was so sensitive and tried arguing, but I know how I reacted and he wasn’t there!

For what it’s worth, a few years after that I used it for 2-3 days and did not have nearly the same amount of rebound insomnia. Maybe that time I was enough more exhausted that the exhaustion beat the rebound.

As an alternative, Sonata is supposed to have a shorter half life and in my case, I had somewhat less of a problem with rebound insomnia (plus it caused less of the “brain dead until noon” hangover).

6

You and your doctor are both correct. Zolpidem is not, based on it’s chemical structure, a benzodiazepine, however, it targets the same binding “pocket” on the GABA-A receptor complex that a benzodiazepine, such as clonazepam, would, albeit much more selectively towards GABA-A containing an interfacing alpha-1 and gamma-2 subunit, versus the alpha-2 or 3 subunits.

I am somewhat curious as to what dose your doctor put you on with the Ambien. The reason I’m curious is that the FDA actually forced a label change last year for almost all zolpidem products because the data suggests that, at the 10mg dose for the immediate release form, about 1 in 5 non-elderly women experience next morning/day cognitive impairment (which may or may not be noticeable by the patient themselves) putting them at risk if they drive the next morning. And due to how it releases the medication over time, the CR form, particularly at the 12.5mg dose, increases this risk to about 1 in 4 men (who don’t seem to display a statistically significant difference at 10mg IR), and 1 in 3 women. Because of that, the FDA approved text in the medication guides which must be dispensed with each fill of a Zolpidem product state that patients who take the CR form should not drive at all the next day. You can guess as to how many people taking the drug chronically actually follow that particular bit of advice.

7

Can translate into plain English s’il vous plaît? Does “more selectively” mean “fewer side effects” ?

8

I have puberty-onset insomnia - I remember being awake at 02:00 in Middle School.
Until 1999, I used ever-increasing dosages of alcohol and Unisom Caplets (the tablets worked so slow I burned them off before they could do anything.

Then I let a MD I trusted to start me on pills (including triazelam (Halycion) - the side effects of which were “brain damage and death”).
Ambien was among the group, but it is NASTY - I could (and, of course did) stay awake after taking it - it does strange things to the brain.
I am now on more benzodiazepines - and will be for the rest of my life.

My record is 3 days without sleep before finally dropping the pill de jour.

Which is worse? Crappy sleep on knowing you will need a pill for the rest of your life. If you life (job, family, social life) can withstand you being dead on your feet from time to time, I’d try to find a way to sleep without a pill.
If you can afford $150/mo =, try Lunesta - it is a sweet, non-benzo which does a wonderful job.

And NEVER mix Ambien with a Benzodiazepine - it is fatal (I was down to 1/2 of it and a benzo, and thought “what the hell”. Completely disoriented, all but blind - the 6-bulb (60 w incandescent) appeared as a faint candle down a deep hole.

If those had been full-strength dosages, I doubt I’d be here - and I am notorious for sedatives, etc. not working, or burning off.

If you’re going to be on a pill, shop around. I happen to like temazepam (another benzo).

9

tl;dr version for those uninterested in the longer version: Provisionally yes, more selectivity will usually result in fewer side effects. It can also result in a greater chance of some unusual other side effects, like sleepwalking and other parasomnias, and may not be any less addictive than the benzodiazepines (in fact, it can be argued to be on par or slightly more addictive).

The GABA type A (heretofore referred to as GABA-A) receptor complex is made up of 5 subunits. There are a huge number of possible subunit combinations since there are six different alpha subunits, at least three beta subunits, at least 3 gamma subunits, and a delta, epsilon, theta, pi, and 3 rho subunits. Happily, the vast majority of subunits tend to combine in roughly the same groupings in various parts of the brain. The most common combination found almost everywhere in the brain is what was once known as the BZ1 (benzodiazepine 1) receptor grouping, which is two alpha-1 units, two beta-(2/3) units, and one gamma-2 unit, in the pattern of an alpha-beta-alpha-beta-gamma ring, with the first alpha unit in said pattern interacting with the gamma unit. Benzodiazepines and the Z-drugs (zolpidem, zaleplon, and (es-)zopiclone) fit into a specific pocket in between the alpha-1 and gamma-2 subunit and favorably improve how well the GABA molecule can bind to and open the GABA-A ion pore.

Zolpidem binds about 10-20x more strongly if the alpha unit is alpha-1 than if it is alpha-2 or alpha-3 (neither benzodiazepines nor z-drugs bind to alpha-4 or alpha-6 containing GABA-A receptors. Ethanol, on the other hand, does bind to extrasynaptic alpha-4-beta(1-3)-delta GABA-A receptors) and it binds around 100x (if I’m remembering correctly) as strongly to alpha-1 as compared to alpha-5 containing GABA-A receptors. The benzodiazepines, in contrast, bind equally well (so far as we currently know) to all known benzodiazepine sensitive combinations (anything with a gamma-2 and alpha-1, 2, 3, and 5 subunit). Thus, zolpidem, at the standard FDA approved doses, is largely selective for GABA-A receptors with alpha-1 subunits, where clonazepam, temazepam, and alprazolam, to name a few benzos, would not be.

This selectivity would then manifest with fewer side effects, in theory, than the traditional benzodiazepines, since it isn’t augmenting GABA transmission at as many receptor subtypes. In practice, this seems to hold true, but does introduce a potentially greater risk of the more newsworthy unusual side effects (sleep-walking/driving/eating/sex). One of the benefits of using zolpidem at FDA approved doses, for example, is that it shouldn’t actually induce much, if any, dependence, since the dependence producing characteristics of benzos are speculated to be linked with alpha-2 and alpha-3 subunit containing GABA-A due to where those type of receptors tend to be located in the brain (amygdala, hypothalamus, striatum, and locus ceruleus, to name a few regions for those interested) and that those types tend to be post-synaptic (the neuron receiving a signal), whereas alpha-1 containing units can be pre-synaptic auto-receptors as well. Of course, no drug is perfect, so while it shouldn’t (at the FDA labelled doses) induce dependence (and the majority of studies back this up), it can still lead to addiction.

Confused about my use of the two underlined terms? Don’t feel bad, the two are often mistakenly conflated, including by many healthcare practitioners, in my experience. Dependence is a state where your body has gotten used to the presence of the drug and has adapted to this presence in myriad ways, resulting in a withdrawal syndrome of some kind if the drug is removed (or it’s effects blocked by an antagonist–in the case of the benzos and z-drugs, that would be an iv medication known as flumazenil). This is often linked to drug tolerance, which is where an amount of drug which once produced an effect is no longer enough to produce that same effect resulting in the need for a larger amount. Note that while they are often linked, tolerance is not necessary for dependence to develop and vice-versa. Addiction is a complex bio-psycho-social disorder characterized by compulsive seeking (craving) or taking, despite the harm it does to the person (and often their circle of friends and family). Addiction is, in essence, a set of maladaptive memories which are unusually powerful in provoking certain habitual behaviors. It can also be thought of as a reward deficit disorder. Addiction is often reinforced by dependence (more specifically, the symptoms of drug withdrawal act as negative reinforcement to keep taking the drug) and many addicts are very tolerant to their drug(s) of choice at the peak of use, but addiction can (re-)occur without either dependence or tolerance being present at all, and one can be extremely tolerant and exhibit dependence to a drug without being addicted (this is very often where I see other healthcare practitioners get it wrong).

Anyways, back to zolpidem. Zolpidem doesn’t do much at normal doses at alpha-2 and alpha-3 subunit containing GABA-A, which are speculated to be the primary receptor forms mediating anxiolytic (anxiety terminating), anti-convulsive (seizure terminating), and autonomic fight-or-flight blunting effects. Since it doesn’t augment these functions, you don’t find a rebound effect (ie heightened anxiety, greater chance of seizures, over-active autonomic nervous system drive) from those on withdrawal of the drug like you can with the benzos. Unfortunately, it still can be addictive because the brain circuitry involved in addiction is different than the brain circuitry involved with dependence. Ordinarily, in a part of the brain known as the ventral tegmental area, GABAergic (GABA releasing) neurons tonically suppress the firing of Dopaminergic neurons which are part of the brain’s reward circuitry, by acting post-synaptically on alpha-2 or alpha-3 subunit containing receptors. This tonic suppression can be countered in a number of ways, one of which is by the presence of too much GABA triggering pre-synaptic alpha-1 containing auto-receptors which signal to the GABA releasing neuron to stop/release less. Unfortunately, since zolpidem augments GABA to be more effective at the receptor, and since it doesn’t bind all that well to the post-synaptic GABA receptors for reasons already mentioned, zolpidem enhances the suppression of the GABA releasing neuron without also somewhat blunting/mitigating that effect by also augmenting post-synaptic GABA suppression like a benzodiazepine would, resulting in the “reward” dopaminergic neuron firing more frequently. While this is, by itself, not enough to cause addiction, the current thinking (or at least, the thinking I’ve read up to this point) is that the over-active firing of these dopaminergic neurons is a very key part of the overall picture involving the neurobiology of the development of addiction.

That’s probably more of an answer than you expected or wanted, but this particular area fascinates me and I couldn’t help myself. :smiley:

10

Out of curiosity, has your doctor considered the possibility of a delayed sleep phase syndrome? The circadian rhythm changes at/after puberty and a significant portion of adolescents (7-16%) exhibit an exaggerated effect, which can persist into adulthood (about 1 in 10 cases of chronic insomnia, according to the American Sleep Association). It is characterized by a difficulty falling asleep at “normal” bedtimes, but if the person is allowed to stay up till they are ready for bed (1-5am), they sleep normally and awaken refreshed later in the morning/early in the afternoon. If not allowed to do what their bodies are physiologically pushing them towards, they end up excessively sleepy.

Antihistamines are generally considered a poor choice for sleep issues anyways. Their effects on SLO (Onset of Sleep Latency) are marginal, at best, and they are pretty much useless for the maintenance of sleep, but still leave most with a degree of extra grogginess for several hours after waking the morning following use (hangover effect). Further, at higher doses (including max labelled doses), first generation antihistamines (Diphenhydramine, Dimenhydrinate, Doxylamine, Chlorpheniramine to name a few) tend to have more anticholinergic effects (acetylcholine transmission augments wakefulness and cognition during the day and is necessary for the flip-flop between Non-REM and REM sleep at night), which further serve to mess with sleep architecture and continuing sleep problems. Likewise, while alcohol tends to, at moderate to high doses (very low doses are generally disinhibitory and may actually make someone feel more awake) make you tired/pass out, due to various effects on your brain and body, you are more likely to develop middle of the night awakenings following use and is strongly recommended against in, well, pretty much anyone with any type of insomnia. You might already know that, of course, but I’m putting it out there for others reading who might not.

:smack: Triazolam, outside of very VERY short term use (or use for anxiety related to various medical procedures, e.g. a CT or MRI scan) for sleep-onset insomnia, is probably the worst choice among benzodiazepines for use in chronic insomnia. It’s incredibly potent effects, coupled with a half-life/duration of action similar to zolpidem (1.5-5.5 hours, roughly, unless cirrhosis is involved) often results in rebound insomnia–sometimes even in the middle of the night the dose is taken, due to withdrawal effects. That being said, outside of doses causing coma, withdrawal seizures, or combination with other sedative agents, neurologically detectable brain damage and/or death are very unlikely with the use of any benzodiazepine or z-drug alone. They can possibly alter functionality of neural circuitry in various brain regions, particularly if used on a chronic basis, but that generally isn’t considered brain damage.

While I agree, for some, Zolpidem can be nasty, it isn’t actually doing all that much differently than the benzodiazepines, in most cases. GABA-A receptors expressing alpha-1 subunits are thought to be the principle subtype involved in mediating hypnotic (and at least some of the cognitive/memory) effects for both the benzos and the z-drugs. Zolpidem is (arguably) slightly more dis-inhibitory than the benzos due to it’s selectivity, which may be why you hear more reports on various zolpidem induced parasomnias (sleep walking, sleep driving, etc) than benzodiazepine induced parasomnias, but otherwise they largely “work” in the same way.

In general, yeah, figuring out and correcting the underlying cause of the difficulty sleeping is the best thing you can do, as well as relying on good sleep hygeine, and cognitive behavioral therapy approaches, rather than relying on a medication to mask the symptoms. The non-pharmacologic therapies and recommendations are safer just by virtue of having few side-effects (many of those probably attributable to the placebo effect).

As for Lunesta, that would be because eszopiclone is essentially a non-benzo benzodiazepine, ie it doesn’t have the benzodiazepine chemical structure but works at the same site of action. It doesn’t even have the receptor selectivity that zolpidem does. It also has a reliably longer half-life in comparison to zolpidem and triazolam (~6 hours; ~9 hours in the Elderly), but is still shorter than the half-life of alprazolam (12-15 hours) so you have less next-morning grogginess following acute use. As an aside, I’m using half-lives, but with this class of medication, it’s important to understand that half-life and duration of effect aren’t the same thing.

Actually, the combination, given the competition for the binding pocket, is rarely fatal, unless it’s combined with another sedative (opioids, particularly acutely). It’s still a very bad idea to combine them (sadly, despite my pharmacist colleagues and mine best efforts to convince them otherwise, some local physicians are doing precisely that to many of our patients, often on top of chronic opioid therapy :smack:), IMO.

11

JayRx1981, thank you very much for taking the time to write all of the above lengthy, detailed, and mostly plain-English posts about all these topics. While the technical details are (mostly) over my head, your explanations are definitely helping to fight the ignorance, at least at a lay level.

Your tangential discussion of the distinctions between dependence, tolerance, and addiction are also helpful. I was never sure just which of those words meant what, and I’ve mis-used those words myself.

I have a background (about 10 years ago) of developing tolerance and dependence with clonazepam, which I had been calling addiction, but now I understand it wasn’t really that. I was in the early-most stage of developing craving (watching my wristwatch for several hours before the next dose time, counting down the seconds until my next fix, trying to resist jumping the gun and taking the next dose early), when I recognized what was going on and quit, cold-turkey. I was using a very minimal dose (IIRC, I had worked up to 0.5 mg b.i.d. and sporadically t.i.d.), and I thought quitting cold-turkey would be no problem.

Wrong.

(Well after the fact, some doctors told me that such a low dosage should have been no problem to quit, and they would have recommended just quitting, without tapering.)

I immediately developed severe withdrawal (no seizures, though) and life got nasty. Worse, it seems I also developed PWS (protracted withdrawal syndrome), said (by Heather Ashton) to occur in about 10% to 15% of cases, in which the withdrawal symptoms persist for months to years. (Is it known how that works?) Bleagh! Since joining this message board, I’ve proselytized regularly against benzos.

Are you familiar with the work of Heather Ashton? Professor of neurology (now retired); ran benzo rehab clinic for many years; wrote popular paper on the topic (as well as numerous juried publications, apparently). Ashton, C. Heather. Benzodiazepines: How They Work And How To Withdraw.

12

I’ve been taking Ambien for a couple years and there is no comparison between how I sleep with it and without it. I’ve always been a REALLY light sleeper with a VERY active bladder and I would normally wake up 2-4 times every single night. It was just normal to me. Miserable but normal.

Then I got a prescription for Ambien, the non-CR version. 10mg. The first night I took it it did absolutely nothing. No effect whatsoever. I was very disappointed. The next night it got me stoned as hell and I slept like a baby for a good 5hr stretch before waking up. I was taking one every few nights for a while but then decided that I was restricting things for no reason. For the last year or so I’ve been taking 5mg every night (split the pill). It’s just enough to get me to sleep quickly but not enough to get me baked. I’ve never had morning hangover grogginess while taking it. Every once in a while the 5mg will still make me a bit loopy, but it’s worth it in the end. I’m not feeling sleepy by 2pm every day like I used to.

If I had to just up and quit cold turkey today it would be hard but I’d survive. I have tried to ease off of it in the past but it’s admittedly hard to do. I don’t feel like I’m addicted to Ambien, but I do find that it’s really hard to voluntarily subject myself to a horrible nights sleep for no real reason, so I guess I’m addicted to the sleep I get while on Ambien. My wife notices a major difference in my mood if I go a couple nights sleeping without.

(Yes I’ve had sleep studies and tried other meds before Ambien etc…)

13

Happy to do it, honestly. I’ve spent a large chunk of time learning about how GABA and opioid transmission works in the brain, where it’s working, what receptor subtypes are believed to be involved (and their binding and open-close kinetics where possible), what the known or suspected mechanisms of tolerance are, etc, primarily because of the sheer volume of prescriptions for medications like benzos and opiates we dispense, and I felt it was my responsibility to know as much as possible to be able to answer my patient’s questions honestly with regards to the benefits versus the risks of these medications. I won’t say I’m anywhere near an expert yet, but I’m certainly pushing myself in that general direction. Also, despite knowing the difference between addiction and dependence, I still sometimes colloquially conflate them, the way most people probably do. Honestly, given how negatively charged the term addiction is, there is now a movement to stop using it and to refer the condition in question as a Substance Use Disorder instead, so I’m actually trying to start referring to it like that.

Based on my reading and anecdotal experience, the dependence issues with benzodiazepines are more likely a function of time you’ve been on the drug versus dosage, until you start getting into higher dose territory. Dependence is argued to develop over about 8-12 weeks, for alprazolam as an example, until/unless you’re dealing with total daily doses of 4mg or more per day, though that’s also going to depend on other factors like how frequently you actually take the drug, if you’re taking it on an as needed basis, or on a scheduled basis, and how much time passes in between each dose among other things.

So with a multi-year history of use, using Ashton’s numbers (in my experience, and I’ve calculated it out for several different patients who were undergoing a switch to a different benzo or were being tapered, her conversion numbers are IMO more accurate than the ones found in other references, like Pharmacist’s Letter), your 1mg of clonazepam works out reasonably well to 20mg of diazepam daily. If we use the Ashton manual as a guide, the recommendation in chapter 2 for someone on, say 40mg a day Diazepam equivalent dose was to decrease by 2mg per day, decreasing further every 1-2 weeks until you hit your 20mg DED, then decrease by 1mg per day from then on out. If you did that at her most rapid recommended pace (1mg DED, dose reduced every 1 week), you’re still looking at 20 weeks (~5 months) before you are off completely, assuming no hiccups. At 0.5mg BID dosing, I can understand why those doctors thought you’d be fine without a taper, I just don’t happen to agree with them (at best, a trial of stopping suddenly to see how you respond with the option to go back on to taper would be a reasonable middle ground).

I’m sorry to hear that. I hope that as time has passed, the PWS symptoms are at least gradually improving or have gone away altogether. The truth is, we don’t yet know for sure what causes them in one person but not another. We might never really be able to say for sure. The problem with teasing out what the benzodiazepines are doing, acutely and chronically, is that the benzodiazepines can actually have different functional effects in different brain structures, despite mechanistically all enhancing the opening of GABA-A Chloride channels. They can simultaneously be augmenting excitatory transmission of dopamine in the ventral tegmental to nucleus accumbens pathway by inhibiting inhibitory interneurons, while augmenting the inhibition of excitatory norepinephrine signals originating in the locus ceruleus. With GABA, we’re talking about the major inhibitory neurotransmitter of the brain (glycine takes that honor in the spinal cord, based on much of what I’ve read, while it takes a back seat role in the brain itself). While the benzodiazepines and z-drugs only augment the function of GABA at a certain subset of GABA-A receptor types (triggering no response in the absence of GABA), and this mostly occurs at the synapse, functionally speaking, they pretty much alter the processing of excitatory signalling at every level of the brain. They have been shown to alter brain plasticity in different ways, enhancing, at least acutely, Long Term Potentiation in the Ventral Tegmental-Nucleus Accumbens circuitry (see this study here), as an example, which could serve to enhance the strength of a maladaptive memory formed in a person at risk for developing an addiction, which would remain even after the use of the drug has ceased.

This is why I’m largely in Ashton’s camp, with regards to their use. I have, barring other contraindications, no problem professionally with their being used short term for insomnia, anxiety, muscle relaxation, and anti-convulsive properties. Used judiciously, like the opioids, they can be incredibly fast and effective at what they do. I’m just not a fan of their long-term (more than 2-4 weeks) use unless no potentially better options exist. There are too many unanswered questions about long-term adaptations in neural function for me to be comfortable recommending them long-term, and most texts and guidelines on the topic recommend the same thing.

See above, but yes, I’m quite familiar with her work.

14

Interesting.

As I mentioned above, I have Restless Legs Syndrome. In the late 1990s and early 2000s, I decided I had to move on from toughing it out (my beloved husband was my enabler in that, massaging my legs until I fell asleep more nights than not). At that point, the main pharmaceutical options (all off-label) were:

  • Benzos (specifically Klonopin / clonazepam)
  • Dopamine agonists such as used for Parkinson’s
  • Neurontin (gapapentin)
  • Opiates

Each of these has its benefits and drawbacks.

I had one neurologist really push me to try Klonopin. I was terrified of benzos, and had heard enough about Klonopin usage for RLS that it sounded like a Very Bad Idea to me. I never went back to that neurologist.

I consulted with a couple of the world leaders in RLS (only an hour or so away from home) and we discussed all the options. Their take on benzos versus opiates was that it was a lot harder to develop a dependence on benzos than opiates - but also a lot harder to get OFF them. Senegoid’s history would seem to support that :(.

15

On the CR form / driving: I wonder if someone taking it longer-term would develop enough of a tolerance that this would not be a problem?

I’m reasonably sure my dosage was 10 mg (this was about 13 years ago so I can’t be sure). I’m a larger person (and non-elderly :D) for what that’s worth. I am absolutely sure that it was NOT a CR formulation - for my situation, the problem was falling asleep, not staying that way, a sustained release version wouldn’t have been necessary.

I do tend to have a longer bounce-back time from any sedation. Last time I had a colonoscopy, the next morning (nearly 24 hours later) I was working from home and staring at the computer bemused at all those words 'n stuff. It was early afternoon before I was functional.

16

If taking the drug isn’t causing home, work, or social life problems, not taking it is causing problems (which can’t be accounted for in other ways, such as a comorbid (fancy way of saying co-occurring) major depressive, anxiety, or pain disorder being exacerbated by the lack of sleep, not the lack of the drug), and you don’t find yourself dose-escalating or compulsively thinking about taking the drug, I’d honestly not be too concerned about addiction. Not to say it isn’t possible, but I would just professionally be more concerned with your safety if you needed to drive or operate heavy machinery in too close a proximity to when you took your nightly dose, and again, the somewhat unknown long term consequences on cognition/memory, than I would be addiction.

Something I remind my patients of regularly is that ALL drugs, OTC or Legend or Controlled substance: ALL have both benefits and risks, and in theory, our job as healthcare practitioners of varying stripes is to help you find the therapy that balances those acceptably for your particular circumstances. More specifically, each of those does have some degree of support for the treatment of RLS (so the neurologist in question wasn’t exactly wrong), but the authors of the chapter on Insomnia in my copy of Principles of Neurology (9th ed), tend to prefer the dopamine agonists as first line over the other options.

Honestly, I don’t think it’s necessarily harder to develop a dependence (substance use disorder/addiction without concomitant use of other drugs of abuse/misuse, on the other hand, certainly) to benzodiazepines, it’s just usually more a function of time of exposure coupled with the ease at which one, patient, physician, or both, can confuse anxiety/periodic-limb-movement secondary to drug withdrawal from an active exacerbation of an anxiety/panic disorder/RLD. I’d agree that benzodiazepines, outside of the very long half-life opioids methadone and buprenorphine, at least based on patient report, are probably a lot harder to actually get off of.

Most of the literature I’ve gone over, where the cognitive effects are mentioned, including but not limited to the works of Heather Ashton, seems to suggest that if it does, it’s over a MUCH longer time-course than any of the other tolerances (sedation, anti-convulsion, myorelaxant, or anxiolytic), similarly to opioid induced constipation, which I was taught when it occurs never goes away, but Principles of Addiction Medicine asserts that it would develop (on a stable dose, mind, since we’re talking opioid addiction maintenance, not pain therapy here) after several years of use. Given theorized benzodiazepine effects in the hippocampus and cortex, I can believe it.

If it was the 10mg dose and accounting for your gender, the response you had at first isn’t all that unusual. For reasons still not completely understood, women clear the drug more slowly than men, which could in theory result in enough exposure to the drug to partially counterbalance it’s poor binding affinity with regards to alpha-2 and 3 containing receptors and result in rebound insomnia. The paucity of details, unfortunately, leaves this as speculation at this point.

17

I don’t recall having much trouble with insomnia before my stint with cloanzepam (this was a bit over 10 years ago), but while I was using, I began to get depending on having my evening fix in order to be able to sleep. It was a weird and unnatural sleep, too, I thought. Ever since I quit, I’ve had trouble with insomnia and irregular sleep.

To be sure, I was subsequently also diagnosed with apnea. But the sleep clinic seemed to act like EVERYBODY has apnea. The mere having of a pulse seemed to be diagnostic of apnea. (I supposed if a patient didn’t have a pulse, that’s apnea too.) I used a CPAP machine for a while, but could never get comfortable with it.

So, despite the long hijack about benzos instead of Ambien, I’m watching this thread with interest for all kinds of reasons. During my benzo withdrawal, with gruesome anxiety and non-stop panic attacks and intense insomnia, I had Ambien to help sleep. I was terrified to use it, so mostly I didn’t.

At one time or another, the doctors (I ended up seeing at least 6 of them) prescribed or recommended (1) Ambien, (2) Trazodone (largish dose, IIRC), (3) Hydroxyzine, (4) Diphenhydramine 75 to 100 mg, (5) mirtazipine (Remeron) and (6) yoga to help me sleep. At best, they worked well for one or two nights, and not thereafter. Well, the mirtazipine worked very well, but began to have its own adverse effects (I think) after a few weeks. And at all times, I was terrified that any drug that helped treat the symptoms of benzo withdrawal would, itself, cause a dependency and withdrawal problems of its own later on, and I didn’t want that to happen!!!

I also went back on the clonazepam in order to settle down my inflamed neurons, then to try tapering like I should have in the first place. (Under a doctor’s supervision this time.) That didn’t work at all. In retrospect, by the time I tried that, I’d have been better to just have stayed quit and toughed it out, which is what I ended up doing anyway for the next 8 months.

I felt so debilitated, I went to live in a board-and-care home for those last 8 months. By then, I felt well enough to set forth on my own again, but even then I didn’t really feel right for another year, and to a lesser extent, not even then. It was sort of an adventure to re-discover independent living (plus the fact that I moved to another city 4 hours away at that time).

18

Let’s get back to ethelbert’s OP. (Remember ethelbert’s OP?)

The parts I’ve bolded closely resemble my experience with clonazepam (which I didn’t mention in my earlier posts). I used it for several months, starting with 1 mg qd PRN, gradually becoming 1 mg qd every day; started getting some signs of dependency; quit cold turkey. NASTY withdrawal ensued, but lasted only about one week.

Fast forward about 6 months: Started using again, even more carefully than before: 0.5 mg qd PRN, gradually increasing to 0.5 mg b.i.d.; then quit again. This is the episode I described in details above, with the 18-or-so month withdrawal.

So I have the same question as ethelbert: Did my earlier experience permanently sensitize my brain so that the later experience would bite me so much worse?

19

The triazalom was attractive BECAUSE it burned of quickly - the problem is getting to sleep; once asleep, I’m good for the night.

Of course 1.5 tabs every night for 2-3 years (a Pharmacist finally got through to the MD and tipped him off re side-effects.

Damage was done - I was a super whiz on computers. Tried a class in SQL (which is really a sub-set of the Mainframe DB2 database) - and could not learn it. Iwas on a project in 1987 in which the “DB2 Expert” could not come up with usable code. Took me an afternoon to pick up the manual and have the code ready to go. Could not even remmeber te command I used for that (“Union”).

Nasty drugs. Am counting down the patent period on Lunesta.

20

If I may tack onto this older thread…

My sleep issue is staying asleep for more than 3-4 hours. Then once I wake my mind starts up and I have a difficult time getting back to sleep. I have no trouble going to sleep at all. If my schedule permits I’m pretty good at napping too.

A couple of years ago my doc suggested melatonin which didn’t seem to do anything at all.

In two weeks I’m leaving for 10 days in Italy. I’ve never had much success sleeping on an airplane either (even though as I mentioned above I’m generally good at falling asleep). So I asked my doctor for something and he gave me 20 ten mg Ambien that I can refill once. I’m not sure if it is the slow release version or not.

Based on the above I’m wondering if I even want to mess with it. I’d rather go thru the trip a little sleep deprived than have a hangover.

I have plenty to experiment with over the next two weeks…any thoughts on how I might do that? Start taking it every night and see what happens expecting my reaction to be consistent for the next three weeks.? Take it once…not take it the next night and see what happens?