A widely prescribed pain medication has been associated with substantially higher risks of developing dementia and cognitive decline, according to new research that examined more than 50,000 patients.
The study found adults taking gabapentin for chronic lower back pain faced a 29 per cent increased risk of dementia and an 85 per cent higher risk of mild cognitive impairment within a decade, compared to back pain sufferers not prescribed the drug.
Gabapentin, an anticonvulsant medication, has become increasingly popular as an alternative to opioids for managing chronic pain due to its lower potential for abuse.
The findings, published in Regional Anaesthesia & Pain Management, have prompted researchers to call for closer monitoring of patients prescribed the medication to check for potential cognitive decline.
Gabapentin users showed a 144 per cent higher risk of dementia
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Researchers from Case Western Reserve University School of Medicine in Cleveland, Ohio, analysed data from the TriNetX national database, creating matched groups of 26,416 gabapentin users and an equal number of non-users.
The team found the risks varied significantly by age group. Among patients aged 35-49, gabapentin users showed a 144 per cent higher risk of dementia and a 250 per cent increased risk of mild cognitive impairment.
Similar patterns emerged in the 50-64 age group, with dementia risk rising by 128 per cent and cognitive impairment by 122 per cent.
The frequency of prescriptions also mattered. Patients receiving 12 or more gabapentin prescriptions showed a 40 per cent higher dementia incidence and a 65 per cent increased risk of mild cognitive impairment compared to those prescribed the medication fewer times.
However, several experts have urged caution in interpreting these findings, pointing to potential limitations in the research design.
“Confounding and reverse causality are tenable explanations for the observed effects,” said Martin Prince, professor of epidemiological psychiatry at King’s College London.
Tara Spires-Jones, director of the Centre for Discovery Brain Sciences at the University of Edinburgh, noted that “while authors used statistical methods to try and account for other risk factors, this type of study cannot prove that gabapentin was the cause of increased dementia risk”.
She highlighted a crucial gap in the research: “One very important factor that was not examined in this study is levels of physical activity. People with chronic pain requiring gabapentin may have been less physically active, which is a known risk factor for developing dementia.”
People with chronic pain requiring gabapentin may have been less physically active
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Sir John Hardy, group leader at the UK Dementia Research Institute at University College London, suggested the findings might be “artefactual and result (for example) from a marginal acute effect on cognitive performance rather than effects on the underlying disease”.
Ian Maidment, professor in clinical pharmacy at Aston University in Birmingham, pointed out that the research failed to account for treatment duration or gabapentin dosage.
He also noted that “other similar recent studies have failed to find a link” between gabapentin and cognitive decline.
“The jury is out on whether gabapentin causes dementia,” Maidment concluded.
The researchers acknowledged their findings provide “a foundation to further research whether gabapentin plays a causal role in the development of dementia and cognitive decline”.
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