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Gabapentin for alcohol use disorder: A good option, or cause for concern?

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Release date: December 1, 2019
Expiration date: November 30, 2020
Estimated time of completion: 1 hour

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ABSTRACT

The anticonvulsant drug gabapentin is used off-label to treat alcohol-related withdrawal, cravings, anxiety, and insomnia. Although it is well tolerated and has demonstrated efficacy for mild alcohol withdrawal and early abstinence, there is concern about its potential for abuse. Gabapentin should be prescribed only as a second-line alternative to standard therapies, and only after screening for opioid or other prescription drug abuse to determine if heightened monitoring is warranted. Clinicians should be aware of gabapentin’s limitations for treating alcohol use disorder and be attentive to emerging data on risks and benefits.

KEY POINTS

  • Gabapentin has been shown to be safe and effective for mild alcohol withdrawal but is not appropriate as monotherapy for severe withdrawal owing to risk of seizures.
  • During early abstinence, gabapentin may improve sleep, cravings, and mood—factors associated with relapse.
  • Gabapentin is being used recreationally to achieve or enhance euphoria, but its misuse potential appears to be low when taken at therapeutic doses by patients without a history of drug abuse.


 

References

Perceptions regarding the use of gabapentin for alcohol use disorder (AUD) have shifted over time.1–4 Early on, the drug was deemed to be benign and effective.4–6 But more and more, concerns are being raised about its recreational use to achieve euphoria,7 and the drug is often misused by vulnerable populations, particularly those with opioid use disorder.7–9

Given the large number of gabapentin prescriptions written off-label for AUD, it is incumbent on providers to understand how to prescribe it responsibly.7–9 To that end, this article focuses on the benefits—and concerns—of this treatment option. We describe the effects of gabapentin on the central nervous system and how it may mitigate alcohol withdrawal and increase the likelihood of abstinence. In addition, we review clinical trials that evaluated potential roles of gabapentin in AUD, discuss the drug’s misuse potential, and suggest a framework for its appropriate use in AUD management.

ALCOHOL USE DISORDER IS COMMON AND SERIOUS

AUD affects about 14% of US adults and represents a significant health burden,1 often with severe clinical and social implications. It manifests as compulsive drinking and loss of control despite adverse consequences on various life domains.10 It is generally associated with cravings, tolerance, and withdrawal symptoms upon cessation. Alcohol withdrawal is characterized by tremors, anxiety, sweating, nausea, and tachycardia, and in severe cases, may involve hallucinations, seizures, and delirium tremens. Untreated, alcohol withdrawal can be fatal.10

Table 1. Agents used to treat alcohol use disorder

Even though psychosocial treatments for AUD by themselves are associated with high relapse rates, pharmacotherapy is underutilized. Three drugs approved by the US Food and Drug Administration (FDA) are available to treat it, but they are often poorly accepted and have limited efficacy. For these reasons, there is considerable interest in finding alternatives. Gabapentin is one of several agents that have been studied (Table 1). The topic has been reviewed in depth by Soyka and Müller.11

GABAPENTIN REDUCES EXCITATION

The anticonvulsant gabapentin is FDA-approved for treating epilepsy, postherpetic neuralgia, and restless leg syndrome.8,12–14 It binds and selectively impedes voltage-sensitive calcium channels, the pores in cell membrane that permit calcium to enter a neuron in response to changes in electrical currents.15

Gabapentin is believed to decrease excitation of the central nervous system in multiple ways:

  • It reduces the release of glutamate, a key component of the excitatory system16
  • It increases the concentration of gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter in the brain7
  • By binding the alpha-2-delta type 1 subunit of voltage-sensitive calcium channels,8,15–17 it inhibits excitatory synapse formation independent of calcium channel activity16
  • By blocking excitatory neurotransmission, it also may indirectly increase the concentration of GABA in the central nervous system16,17
  • It modulates action of glutamic acid decarboxylase (involved in the synthesis of GABA) and glutamate synthesizing enzyme to increase GABA and decrease glutamate.17

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