Across 12 studies encompassing more than 5,000 bariatric surgery patients, neurological complication rates ranged from 1.4% to 16%, with peripheral neuropathy the most common manifestation. Thiamine (vitamin B1) deficiency was the primary driver, particularly of serious central complications such as Wernicke encephalopathy. Mononeuropathies including carpal tunnel syndrome appeared prominently in several cohorts. Timing split into two distinct windows: early compression-related events and later nutritionally mediated deficits emerging years post-surgery.
This review fills a genuine gap. Bariatric surgery's metabolic and cardiovascular benefits are well-documented — it reduces mortality, achieves T2D remission, and cuts cardiovascular risk — yet neurological sequelae rarely feature prominently in pre-operative counselling. The thiamine connection is well-established biochemically, but the 1.4–16% incidence range signals that detection and reporting remain inconsistent across centres, which is itself a finding worth heeding. Wernicke encephalopathy, while less frequent, carries devastating potential; its association with delayed or inadequate thiamine supplementation after malabsorptive procedures is entirely preventable. The review's key practical signal is that structured, long-term nutritional follow-up — not just routine supplement prescribing — is protective. Limitations include heterogeneous study designs, variable follow-up durations, and likely underreporting in routine clinical data. As an incremental but clinically useful synthesis, this systematic review strengthens the case for mandatory post-bariatric neurology screening protocols and rigorous supplementation adherence, information adults considering weight-loss surgery should discuss explicitly with their surgical team.