e23152 Background: Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting toxicity for breast cancer patients that leads to early treatment discontinuation and worse outcomes. Neuromuscular ultrasound (NMUS) is a non-invasive assessment of peripheral nerves that has not been studied in taxane CIPN. Methods: This cross-sectional study enrolled breast cancer patients with subjective complaints of CIPN symptoms during or after taxane chemotherapy and compared nerve cross-sectional area (CSA) by NMUS with historical values in 120 healthy adults. Findings were correlated with self-reported symptom scale (EORTC-QLQ CIPN20, range 0-72, higher more severe); nerve conduction studies; and skin biopsies for intraepidermal nerve fiber density (IENF). Results: We evaluated 20 participants (mean 55.4 ± 10.5 yrs) with NMUS at 74 nerve sites after median 3.7 months (IQR 1.0-6.1) since last taxane (paclitaxel 10, docetaxel 8, nab-paclitaxel 2). Participants reported moderate-to-severe CIPN symptoms which were predominantly sensory (19.1 ±4.9, max 32) as opposed to motor (15.6 ±5.8, max 32) or autonomic (3.3 ±1.6, max 8). Sural sensory nerve CSA was 1.2 mm2 smaller than in historical controls (4.1 vs. 5.3 mm2, 2-sample t-test p = 0.005) and decreased with more days from last taxane (Spearman’s r -0.46, p = 0.04). Tibial motor nerve was not significantly different from controls (p = 0.35). Median nerve CSA was enlarged at the distal wrist crease entrapment site (12.5 vs 10.1, p = 0.03). Older age was associated with smaller sural CSA (r = -0.72, p < 0.001). When controlling for age and days from last taxane, for each 1mm2 decrease in sural CSA, distal IENF reduced by 2.1 nerve/mm2 (p = 0.04, R2 = 0.30). Conclusions: NMUS showed expected sensory predominant distal axonopathy in taxane CIPN. Evaluation of nerve CSA by non-invasive NMUS may serve as an objective point-of-care assessment to risk-stratify women with taxane CIPN prior to the development of debilitating symptoms. Clinical trial information: NCT03139435. [Table: see text]
Potassium Channel Subtypes that Regulate Airway Vagal Sensory Nerve Excitability
