What are the clinical signs of pregabalin toxicity and its recommended management?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 19, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Clinical Signs of Pregabalin Toxicity

Pregabalin overdose primarily causes central nervous system depression manifesting as reduced consciousness, somnolence, dizziness, confusional state, agitation, and restlessness, with more severe cases progressing to coma requiring mechanical ventilation. 1

Primary Clinical Manifestations

Neurological Signs

  • Reduced consciousness and altered mental status are the hallmark features, ranging from confusion to deep coma 1, 2
  • Somnolence and dizziness occur in a dose-dependent manner and represent the most common adverse effects even at therapeutic doses 3, 1, 4
  • Myoclonic movements can develop, particularly in patients with renal impairment, and may occur even without drug accumulation 5
  • Seizures have been reported in overdose situations 1
  • Agitation, restlessness, and confusional states are frequently observed 1

Cardiovascular Manifestations

  • Heart block has been documented in overdose cases 1
  • Cardiovascular stability is generally maintained in most cases, even with significant overdoses 2, 6

Psychiatric Symptoms

  • Depression and anxiety may paradoxically worsen 1
  • Encephalopathy can develop, particularly when combined with myoclonus 5

Time Course and Severity

Clinical deterioration typically occurs 3 hours post-ingestion, even when patients initially appear asymptomatic 2. The onset of adverse effects is most frequently detected in the early days of pregabalin therapy 7.

Peak pregabalin concentrations associated with significant toxicity range from 13-66.5 mg/L, though toxicity severity does not always correlate directly with serum levels 2, 6, 5.

Risk Factors for Enhanced Toxicity

Concomitant Medications

  • Opioid co-administration significantly increases the incidence of somnolence and dizziness 7
  • CNS depressants (benzodiazepines, other sedatives) potentiate toxicity and have been implicated in fatal overdoses 1, 7, 6

Patient-Specific Factors

  • Renal impairment increases risk, though myoclonic encephalopathy can occur even with therapeutic pregabalin levels in acute renal failure 5
  • Elderly patients are at higher risk for serious adverse effects including falls, confusion, and sedation 3

Management Approach

Immediate Supportive Care

There is no specific antidote for pregabalin overdose; management is entirely supportive 1.

  • Airway protection is paramount: Endotracheal intubation and mechanical ventilation may be required for patients with significant CNS depression 1, 2
  • Monitor vital signs continuously and observe clinical status closely 1
  • Contact Poison Control for up-to-date management guidance 1

Decontamination Considerations

  • Gastric lavage or emesis may be attempted if presentation is early, with appropriate airway precautions 1
  • These interventions are only useful within the first 1-2 hours post-ingestion given pregabalin's rapid absorption 4

Enhanced Elimination

Hemodialysis removes approximately 50% of pregabalin in 4 hours and should be considered in severe cases 1. However, multiple case reports demonstrate successful management with supportive care alone, even with very high serum concentrations (up to 66.5 mg/L) 2, 6.

The decision to pursue hemodialysis should be based on clinical severity rather than serum levels alone, as patients with significant toxicity have recovered with conservative management 2, 6.

Specific Interventions

  • Discontinue pregabalin immediately upon recognition of toxicity 5
  • Withdraw or reduce doses of concomitant CNS depressants, particularly opioids 7
  • Myoclonus typically resolves within 24 hours of drug discontinuation with supportive care 5
  • Full neurological recovery generally occurs within 48 hours 5

Critical Pitfalls to Avoid

  • Do not assume cardiovascular or respiratory stability will persist: Patients may initially appear well but deteriorate hours later 2
  • Do not rely solely on serum pregabalin levels to guide management decisions, as clinical toxicity can occur at therapeutic concentrations in certain populations 5
  • Do not overlook polypharmacy: Deaths have occurred with pregabalin in combination with other CNS depressants, though lone pregabalin overdose fatalities are rare 1, 6
  • Do not abruptly discontinue pregabalin in chronic users outside the acute overdose setting, as withdrawal symptoms may occur 4

References

Research

Significant pregabalin toxicity managed with supportive care alone.

Journal of medical toxicology : official journal of the American College of Medical Toxicology, 2010

Guideline

Management of Pregabalin-Induced Dizziness

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

A case of pregabalin intoxication.

Psychiatrike = Psychiatriki, 2012

Related Questions

How should pregabalin toxicity be managed in a patient with acute renal failure (ARF)?
What are the considerations for prescribing Lyrica (pregabalin) to elderly patients with potential impaired renal function and a history of cognitive impairment?
Does pregabalin prescription require laboratory monitoring, including complete blood count, electrolytes, creatinine, and liver function tests?
What are the chances of reversing disautonomia, central sensitization, and gating dysfunction in a 37-year-old patient with a history of benzodiazepine and pregabalin use, impaired renal function, and current fluvoxamine treatment?
How should I manage pregabalin toxicity in a patient with acute renal failure and worsening heart failure?
In a 50-year-old male smoker with a 20‑year smoking history, hypertension, normal BMI, and markedly elevated low‑density lipoprotein (LDL) cholesterol, what is the most effective initial intervention to reduce his cardiovascular disease risk?
What is the safest evidence‑based antidepressant for a patient with Parkinson’s disease who is experiencing depressive symptoms?
In a 50‑year‑old male smoker with hypertension, LDL cholesterol of 8.7 mmol/L and BMI 21, what is the most effective first step to reduce his cardiovascular disease risk?
How should red‑man syndrome caused by vancomycin be managed?
What is the recommended tetanus toxoid (TT) dose, injection site, and immunization schedule for children?
How should I manage pregabalin toxicity in a patient with acute renal failure and worsening heart failure?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.