Fact check: Can ivermectin cause neurological side effects in humans?

1. A systematic review sounded the alarm on real-world severe neurotoxicity

A 2022 systematic review compiled case reports and series documenting severe neurotoxicity from oral ivermectin, including consciousness disorders, seizures, and coma, primarily in patients with heavy Loa loa microfilarial burdens but also in other contexts; the review emphasized that ABCB1 (P‑glycoprotein) mutations or functional impairment can allow ivermectin to cross the blood–brain barrier, producing CNS toxicity otherwise rare at therapeutic exposures ^[1]. This review places human neurotoxicity not as isolated anecdotes but as a reproducible clinical pattern linked to identifiable biological mechanisms, underscoring the importance of parasite burden screening in endemic areas and consideration of host transporter genetics when evaluating adverse events.

2. An alarming single-patient case shows dose and formulation matter dramatically

A detailed 2024 case report described a patient who received intravenous veterinary ivermectin for COVID‑19 and developed severe neurological deterioration, including altered mental status, quadriparesis, and myoclonus; measured serum ivermectin concentrations were nearly five times higher than expected, implicating dose formulation and route in toxicity risk ^[2]. This case demonstrates that off‑label administration routes and formulations designed for animals can produce supra‑therapeutic exposures that precipitate acute neurotoxicity, and it provides direct clinical evidence that excessive systemic levels — not only host susceptibility — can drive central nervous system effects.

3. Animal experiments highlight plausible mechanisms and chronic‑use signals

A 2025 rat study showed that repeated oral ivermectin induced locomotor and neuropsychiatric disturbances, with biochemical findings of acetylcholinesterase and Na+/K+-ATPase inhibition and markers of oxidative stress, suggesting mechanistic pathways for behavioral and motor effects ^[3]. While animal models do not map perfectly to humans, these results outline biologically plausible mechanisms whereby prolonged or repeated exposure could impair neuronal function, and they caution against assumptions that short-term safety in humans automatically extends to chronic or nonstandard regimens.

4. Reconciling diversity of evidence: who is at risk, and why does context matter?

The combined evidence shows three converging risk pathways: very high systemic concentrations (e.g., intravenous veterinary misuse), parasite‑related interactions (heavy Loa loa microfilaremia), and host transporter or biochemical vulnerabilities (ABCB1 mutations, enzymatic inhibition, oxidative stress). Each pathway alone can elevate CNS exposure or susceptibility; together they explain why ivermectin is generally safe at approved doses for on‑label uses yet capable of causing severe neurologic harm in specific contexts ^{[1] [2] [3]}. Public health responses must therefore balance ivermectin’s therapeutic roles against these concentrated but serious risks.

5. Practical implications: screening, formulation caution, and research gaps

Clinicians should avoid nonapproved formulations or routes, particularly intravascular veterinary products, and screen for risk factors such as residence in Loa loa–endemic areas or signs of transporter deficiency when adverse neurologic signs emerge ^{[2] [1]}. The animal work signals a need for studies on long‑term human exposure and mechanistic research into cholinergic and ionic pump effects ^[3]. Policymakers and practitioners must communicate that routine, approved dosing for validated indications carries low risk for CNS toxicity, but off‑label use, overdose, and certain biological contexts materially raise that risk.