What documented case reports exist of neurological toxicity after ivermectin when taken with statins?

1. What the published case series actually report

A widely cited review and case series examining serious neurological adverse events after ivermectin explicitly notes that several individual cases reported concomitant use of drugs that are substrates for CYP3A4 and P‑glycoprotein, and lists statins as one such class (identified specifically in “case 12”)—but the paper does not present detailed clinical follow‑up proving causation by statin co‑administration, and frames these reports as hypotheses that merit further study rather than definitive evidence ^{[1] [6]}.

2. Pharmacovigilance databases show signals but not causal proof

A systematic pharmacovigilance analysis searching the WHO VigiBase found clustered reports of serious neurological events after ivermectin in various settings and geographies, especially in the context of Loa loa co‑infection in Africa, but these analyses report suspected adverse event reports rather than adjudicated causal links and do not single out statin co‑use as a reproducible cause across reports in the publicly available summary ^[3].

3. Mechanistic plausibility—how statins could plausibly matter

Mechanistic commentary in the literature points to two biologic routes that make drug–drug interactions plausible: many statins and other commonly used drugs are CYP3A4 substrates and can be P‑glycoprotein substrates, and P‑glycoprotein function at the blood‑brain barrier normally limits ivermectin CNS penetration—thus inhibition or competition at these pathways could in theory increase central nervous system exposure to ivermectin and precipitate neurotoxicity ^{[1] [5]}. Narrative reviews of drug interactions note the importance of monitoring combinations that affect neurologic function, though they do not offer case‑level proof that statins have caused ivermectin encephalopathy in humans ^{[7] [8]}.

4. What the clinical case reports and series show about timing, dose, and susceptibility

Published human case reports of ivermectin neurotoxicity emphasize overdose, supratherapeutic self‑medication, or host susceptibility (e.g., ABCB1/ABCB1 nonsense mutations) as clear risk contexts; several single‑patient reports describe coma and prolonged neurologic signs after standard or supratherapeutic doses in patients with ABCB1 defects, while case series note other concomitant drugs without proof that those drugs were causal—this means statin co‑use appears as a recurring observation in sparse reports rather than as a replicated causal finding ^{[4] [9] [10]}.

5. Alternative interpretations, limits of the evidence, and reporting agendas

There are alternative explanations for the co‑occurrence of statins and neurologic events—statins themselves have been associated with reversible cognitive complaints in post‑marketing reports, and ivermectin adverse reports often occur in complex clinical contexts (polypharmacy, infections, overdose) that confound attribution ^[11]. The literature cited frames statin co‑use as a plausible confounder or interacting factor worthy of further pharmacokinetic study rather than as established proof; some reporting—especially during the COVID era—has emphasized ivermectin harms or safety depending on advocacy stance, which can skew focus away from careful causality assessment ^{[9] [3]}.

6. Bottom line for clinicians and investigators

Documented case‑level proof that statins plus ivermectin produce neurological toxicity in humans is limited to observational mentions (e.g., statin noted among co‑medications in a specific case in the Chandler review) and signal detection from pharmacovigilance systems; no robust, reproducible case series or mechanistic human study in the provided sources conclusively establishes statin–ivermectin neurotoxicity, and the literature calls for targeted pharmacokinetic, genetic (ABCB1/mdr‑1) and interaction studies to clarify risk ^{[1] [3] [5]}.