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Propofol–remifentanil and the ankle clonus test in scoliosis patients

Ankle clonus can be elicited in more than 80% of patients during emergence from inhalational anaesthesia [1–3]. The inability to elicit clonus during emergence has been described as a useful test for predicting neurological compromise of the spinal cord during spinal surgery [1]. We examined the incidence of inducible ankle clonus during emergence from propofol–remifentanil anaesthesia. Following institutional ethics committee approval and written informed consent, 30 patients aged 15–20 years, of ASA physical status 1–2, underwent surgical correction of idiopathic scoliosis. A target-controlled infusion pump (Fresenius Orchestra Base Primea; Fresenius Kabi, Bad Homburg, Germany) was used to deliver propofol and remifentanil. During surgery, the patients’ lungs were ventilated and anaesthesia was maintained with propofol at effect site concentrations of 3.0– 5.0 lg.ml and remifentanil at effect site concentrations of 2.0–6.0 ng.ml, with intermittent doses of rocuronium. At the end of surgery after neuromuscular transmission returned, as evaluated by train-of-four peripheral nerve stimulation, the propofol infusion was discontinued while maintaining the remifentanil at 1.0 ng.ml. With every decrease of 0.1 lg.ml of propofol, we performed an ankle clonus test until patients opened their eyes in response to verbal command. Bilateral ankle clonus was elicited in only 40% of patients (12 ⁄ 30), and no patients had demonstrable neurological impairment postoperatively. The median (IQR [range]) propofol effect site concentration for a positive ankle clonus test was 2.1 (2.4–1.7 [2.7– 0.7]) lg.ml. There have been no studies investigating the validity of the ankle clonus test during propofol–remifentanil anaesthesia, although this type of anaesthesia has benefits such as rapid recovery, minimal postoperative confusion and minimal effects on somatic evoked potentials [4]. During emergence from general anaesthesia, lower motor neuron function returns before cortical inhibitory impulses regain their normal function; this disinhibits lower motor neurons thereby allowing clonus to occur during testing [5]. Spinal reflex responses are suppressed at low concentrations of propofol and reflex activity of the spinal cord is less pronounced during propofol anaesthesia compared with sevoflurane anaesthesia [6, 7]. This suggests that propofol may more potently inhibit the appearance of ankle clonus compared with volatile anaesthetic agents. The limitations of our study include that there were no controls and the observers were not blinded to the study protocol. Our results suggest that anaesthesia maintained with propofol and remifentanil may suppress ankle clonus during emergence, thereby making it of limited use as a marker of spinal cord impairment.