gabapentin

General Information

Gabapentin is an anticonvulsant/neuropathic pain medication (brand Neurontin) approved for adjunctive therapy in partial seizures and for postherpetic neuralgia (label). In psychiatric care it is sometimes used off label as a sedating adjunct for anxiety symptoms or sleep maintenance—particularly when clinicians are trying to avoid benzodiazepines or when comorbid pain is prominent.

Evidence for anxiety disorders is mixed. Gabapentin may help with physiologic hyperarousal and somatic tension in some patients, but it is not a first-line long-term treatment for generalized anxiety disorder, panic disorder, or PTSD compared with psychotherapy and SSRI/SNRI-based strategies.

The clinical “cost” is often sedation, dizziness, and gait instability. These effects can be substantial in older adults and in serious mental illness where polypharmacy and baseline neurologic impairment are common.

Gabapentin is not appreciably metabolized and is cleared renally as unchanged drug; renal function is the key determinant of safe dosing. When eGFR declines, dose accumulation can present as ataxia, confusion, and falls.

Misuse/diversion risk has increased in recent years. Treat escalating dose requests, lost prescriptions, or co-use with opioids/other sedatives as signals to reassess risk and to tighten prescribing controls.

The gabapentin compare view, gabapentin evidence feed, and gabapentin print page can support aligning anxiety/sleep adjuncts with sedation and misuse risk.

Because gabapentin is inexpensive and often perceived as “safer than benzos,” it can become a default PRN sedative without clear targets or follow-up. Use is often kept indication-specific (sleep maintenance, nocturnal anxiety, somatic tension, pain-related insomnia) and reassessed within weeks; sedation, falls, and misuse/diversion are monitored.

Mechanism of Action

Refer to the Glossary entry on Neurotransmitters for background on receptor systems involved in serious mental illness.

Binds the α2δ subunit of voltage-gated calcium channels, reducing calcium-dependent release of excitatory neurotransmitters. It does not directly bind GABA-A receptors despite the name.

Clinical “calming” effects likely reflect reduced hyperarousal and improved sleep continuity rather than direct anxiolysis; patients often describe less somatic tension and fewer nighttime awakenings.

Because the primary effect is sedating, response should be interpreted through a safety lens: if anxiety relief comes at the cost of daytime impairment or falls, alternative strategies are preferred.

• α2δ calcium channel ligand (primary).
• No clinically meaningful CYP enzyme inhibition/induction.

Metabolism and Pharmacokinetics

• Not appreciably metabolized; eliminated renally as unchanged drug (label).
• Apparent elimination half-life is ~5–7 hours; regular dosing is often divided (BID–TID) (label).
• Clearance is proportional to renal function; dose reduction and/or longer intervals are required in renal impairment (label).
• Sedation and ataxia are common “toxicity signals” when dosing exceeds the patient’s clearance; eGFR reassessment is common when symptoms emerge.

Dosing and Administration

• In psychiatric practice, a bedtime dose is often used initially for sleep maintenance or nocturnal anxiety, with slower titration based on next-day sedation and dizziness.
• If daytime dosing is used for persistent somatic anxiety, daytime doses are added cautiously and driving/fall risk is reassessed; gabapentin is often not framed as an indefinite “PRN calming” medication.
• Dosing is adjusted for renal function and the plan is revisited after acute illness, dehydration, or medication changes that may reduce clearance.
• Abrupt stopping after sustained daily use can trigger rebound insomnia/anxiety and withdrawal-like symptoms; tapering is commonly used.

Monitoring & Labs

• Renal function (eGFR/CrCl) before starting and after clinical changes that may reduce clearance.
• Sedation, dizziness, gait instability, and driving/fall risk during titration.
• Reassess for peripheral edema and weight changes over weeks to months.
• Misuse/diversion signals (early refills, dose escalation, co-use with opioids/alcohol).
• Tapering rather than abrupt stopping after sustained daily use.

Sources: FDA/DailyMed label; anxiety disorder review; misuse/diversion systematic reviews.

Adverse Effects

Interactions

• Additive sedation/respiratory depression with opioids, benzodiazepines, alcohol, and other CNS depressants.
• Antacids containing aluminum or magnesium can reduce absorption; separate dosing is often separated when feasible (label).
• Few CYP interactions because gabapentin is not appreciably metabolized; medication reconciliation often focuses on sedation burden and renal clearance.

Other Useful Information

• If gabapentin is used for insomnia symptoms, define the target (sleep onset vs sleep maintenance) and reassess within weeks; indefinite nightly use without a plan is generally avoided.
• Alternatives are often considered first in patients with high fall risk, cognitive impairment, or concurrent opioid therapy; if used, lower starting doses and limited quantities are common.
• For anxiety, gabapentin is typically treated as an adjunct to psychotherapy and SSRI/SNRI strategies, not a replacement.

References

1. Gabapentin prescribing information (Neurontin) — DailyMed (2026)
2. Gabapentin and Pregabalin for the Treatment of Anxiety Disorders — Clinical Pharmacology in Drug Development (2018)
3. Treatment of Social Phobia With Gabapentin — Journal of Clinical Psychopharmacology (1999)
4. Gabapentin misuse, abuse and diversion: a systematic review — Addiction (2016)
5. Abuse and Misuse of Pregabalin and Gabapentin: A Systematic Review Update — Drugs (2021)