Report from the field: once in my 40 years of practicing general psychiatry I was able to use gabapentin to help withdraw a patient from clonazepam. Subsequently she reported being "addicted" to gabapentin and stopped seeing me....she NEVER reported either clonazepam or gabapentin causing euphoria....

One anecdotal report...but I have been assuming GABA was involved.....

Article Gabapentin Withdrawal: Case Report in an Older Adult and Rev...

Hi Devin!

Please see the attached document on gabapentin misuse alone.

Numerous articles have been published in medical journals about the recreational potential of gabapentin in the last decade. The consensus is that gabapentin has low abuse potential.

But gabapentin can elicit euphoria, altered mental states, and disassociation in some users. Recreational gabapentin users have also reported that this anticonvulsant helps alleviate benzodiazepine and/or opiate withdrawal.

The first case report of gabapenten recreational use was published in 2007. The authors describe a 67 year-old woman with comorbid depression and alcoholism who escalated her dose to 7.2 grams per day. She obtained extra gabapentin by lying to pharmacists and purchasing gabapentin over the internet.

When she could no longer obtain gabapentin, she developed a withdrawal syndrome characteristic of this class of medication:

trembling

sweating

excitation

pallor

exopthalmia (protrusion of the eyeballs)

Gabapentin users have reported a range of subjective experiences:

Euphoria (Golden Bliss of the World)

Enhanced sociability

A state of relaxation, but also “zombie-like” effects

A sedative/opiate-like buzz with no discernible comedown

Psychedelic / MDMA-like effects.

Thank you Ranjita.  I am interested particularly in the "subjective experiences" that your patients reported re: gabapentin.  I am wondering if these subjects were using ONLY gabapentin or were mixing it with other substances (e.g. alcohol as in the case you mention)?  This is because, as I am sure you are aware, it is hard to construct a pharmacokinetic theory of how gabapentin might induce, say, euphoria BY ITSELF [pts with extreme anxiety might *report* euphoria when in fact they are experiencing relief from extreme anxiety - hard to distinguish, one might imagine, but different].  On the other hand, it is clear that gabapentin (like other neuroleptics including benzodiazepines, pregabalin, and other meds that up regulate GABA in the amygdala) have a POTENTIATING effect -- opioid users, for example, regularly use even weak neuroleptics such as diphenhydramine (Benadryl) to potentiate such substances.  I suppose my intuitive view is that gabapentin is quite safe and that encouraging prescribers to curtail its use might have unintended consequences -- that is, pts might resort to much more dangerous substances (strong opioids etc).  I think most clinicians would rather have their patients using gabapentin than diacetylmorphine - no?  I have found no large scale, statistically significant studies that show that gabapentin ALONE induce any truly dopa-ergic effects (e.g. euphoria, stimulation, "buzz") but rather studies that examine small cohorts of polysubstance users, one of which happens to be gabapentin.  [Of note is the meta-study a few months back in ADDICTION - Society for Study of Addiction, UK - but when you examine the underlying studies, most are again clouded by other substances and so-forth].   I agree with Smith, et al [the article you attached] that there is demand from substance users for gabapentin - so clearly it is of some utility and may have some potential for overuse - but still the data seems clouded.  A street value of 1 GBP/300mg indicates that value - but it does not prove that gabapentin alone is a euphoriant, and it does not disprove that gabapentin has that value because it is a good substitute for, say, benzodiazepines, which are harder to obtain (in volume).  It may be a substance of "last resort" - who knows what engenders the utility to the user -- it may be more of a defensive medication, say against detox from other substances (like buprenorphine, which also has a high street value but a relatively low "euphoria index" compared to full opioid agonists)?

I would be most interested if you can think of how gabapentin could up regulate, say, dopamine - or a metabolite that could bind to opioid receptors, or some mechanism of action by which gabapentin BY ITSELF could do anything other than act as an anxiolytic/neuroleptic.

Best regards,

Devin

Hi Devin- 

I am glad you are pursuing this question. I think it is important that professionals acknowledge the "abuse potential" of any substance through a menagerie of lenses, rather than just one or two. I hypothesize that people who use substances, as well as people in partial or full remission from substance dependence, will have varying perceptions of drug-induced euphoria, mediated by so many factors, interpersonal, neurological, or environmental, that could be confounding to determining a concrete dopa-ergic value. This, I offer as a caveat for some personal experience. 

I am a person in long-term recovery from substance use and made sure my provider knew this when I sought non-hormonal relief from hot flashes. She prescribed Gabapentin (off label) but warned me that it could make me very groggy until I was beyond titration. I had doubts not because of my recovery status, but because of my busy lifestyle and early morning routines. 

At the time I was unaware of "gabbies" having any concerning properties, although some quick preliminary research indicated that, surprisingly, they had street value in the UK. I concluded that was a culturally normative circumstance, and that my physician likely knew better than me,  so I obliged and waited for a weekend to start the protocol.

After I took my first dose, I experienced notable euphoria while falling asleep, slept very hard, and had a very difficult time waking on the following morning. The "rush" was enough to make me question whether I would take the prescription again or find another alternative to mitigate my hot flashes. I determined that I would not take them again. 

I will admit that what I experienced as euphoria may have just been mildly relaxing to someone else. I acknowledge that my well-established, full remission from substance use could have augmented the perceived effect of the drug. I will also say, however, that I had no expectancy for an effect, other than fatigue. Additionally, prior to recovery I had, historically, a low tolerance to narcotics, and required very little to achieve effect. I was a garden variety alcoholic, so I seldom mixed anything because that was dangerous. Perhaps my cognitive awareness (latent fears) of my status as a person in long term recovery augmented the effect from an arousal standpoint. What I can tell you is, that in layman's terms, I experienced euphoria when I took the RX, by itself, with no current hx of any other mood/mind altering substances.  

I know you were asking for Physician's reports of pt's self-reports, but it was that very experience that has called me to learn more about Gabapentin (as well as Tramadol). I will be following your thread for sure!  It will be interesting to see how this subject gets deconstructed and hypothesized in the neurological, social, subjective, and cultural domains. 

Thanks :) 

Jenna 

Jenna,

Thank you for your candid report.  It is very interesting and informative, yet raises further questions about the neurophysiology behind the euphoria you experienced post ingestion of (300mg/600mg?) of gabapentin.  I am not aware of any research that explains this, and looking and the pharmacokinetics of gabapentin and pregabalin (its stronger cousin, similar mechanism of action) I am perplexed as to how this euphoria is induced.  Tramadol *is* an opioid, that is, it has (weak but material) binding affinity to the mu and kappa opioid receptors, so it is nothing to be sanguine about.  Certainly, pts in recovery from opioid use disorder should probably avoid it, especially as a long-term treatment for pain. 

But gabapentin, pregabalin, and the benzodiazepines, for that matter, have as their *primary* action increasing GABA levels in the amygdala, which has the effect of SLOWING DOWN, not speeding up, neurotransmission, not just of dopamine, but of the other in the "big four", including glutamate, serotonin, and norepinephrine.  

But by the same token, there are plenty of reports of pts experiencing "euphoria" (what exactly that means is obviously subjective and thus we don't know it is the same thing, e.g. for some with severe anxiety, "euphoria" may mean the absence of that mental pain, not the presence of a new stimulus) with benzos.  However, this tends to diminish very rapidly with use -- that is, for the first few days a pt is prescribed, say, clonzepam, they may experience mild "euphoria" within 90 minutes after PO administration, but it fairly quickly wanes and just becomes a purely neuroleptic feeling.  

Do you think that most gabapentin users continue to experience this euphoria over time, or does it dissipate quickly (e.g. well before tolerance to neuroleptic effects develops)?

Thanks for the info -- yours is the first actual pt report I have seen of pure (that is, non-polysubstance) induction of euphoria with gabapentin.  If it weren't off-patent, someone would fund a study.  I wonder, given street value and even a nickname, if the DEA is looking into scheduling gabapentin (it scheduled pregabalin as V, which as I'm sure you know means technically that the states get to decide whether it is a controlled substance.)  The DEA may not be great at everything, but they are surprisingly good at assessing the potential for addictive properties.  I wonder if they are reconsidering gabapentin, and if so if it is based on neuroscience, pt reports, or their own proprietary research (which is notably quite good).  Would be interesting to ask them.

Thanks again,

Devin