Ropivacaine, a new local anesthetic agent with a chemical structure very similar to bupivacaine, was not initially marketed to be delivered by the intrathecal route. However, the recent demonstration of lidocaine-associated TNS has stimulated the search for alternative drugs.

Comparing the potencies of local anesthetic agents in the intact subject is challenging because the most rigorous definition of potency is found by testing an isolated nerve in a controlled laboratory setting. Nevertheless, to the clinician, duration is an important and practical indication of potency. Epidural studies have indicated that ropivacaine is between 20% and 40% less potent than bupivacaine [2-5].

When administered by the intrathecal route, ropivacaine is clearly less potent than bupivacaine at the same dose. Because the characteristics of the spinal block produced by 8 mg bupivacaine are similar to those seen with 12 mg ropivacaine, the current study suggests that ropivacaine is 50% less potent than bupivacaine when administered intrathecally. Interestingly, several early reports on epidurally administered ropivacaine suggested that this new drug produced less motor impairment than bupivacaine. The results of this current investigation by Gautier and colleagues argue strongly against a specific drug effect and favor instead a potency-related effect. In other words, ropivacaine is associated with less motor impairment than is produced by the same dose of bupivacaine because ropivacaine is less potent.

The issue of TNS is a fascinating one. Hampl defined this entity as pain, or dysesthesia, or both in the buttocks, thighs, or lower limbs beginning after recovery from spinal anesthesia and typically resolving within 72 hours [6]. TNS are especially common after the use of lidocaine. Concentration and baricity do not seem to be important determinants because TNS are as likely in patients receiving 2% isobaric lidocaine as in those receiving 5% hyperbaric lidocaine intrathecally. It does, however, appear that surgical positioning (lithotomy or arthroscopic knee surgery with stretching of the sciatic nerve) has an effect on the incidence of TNS.

A recent study by Freedman and colleagues of almost 2,000 patients explored the issue of TNS after spinal anesthesia [7]. The investigators found that TNS were common after lidocaine, and relatively uncommon after bupivacaine or tetracaine. The lithotomy position and outpatient status were important risk factors, with the likelihood of TNS ranging from 3.1% for supine inpatients to 24.3% for outpatients in the lithotomy position. Neither age, gender, history of back pain, lidocaine dose or concentration, needle size or type, aperture direction, sitting position during intrathecal injection, nor addition of epinephrine in patients given lidocaine affected risk.

Concerns about lidocaine have led to the re-examination of the older short-acting drugs, such as prilocaine or mepivacaine, for outpatient surgery and have also stimulated attempts to adapt the longer-acting local anesthetic, bupivacaine, to ambulatory surgery. A growing body of literature suggests that spinal anesthesia adequate for day surgery can be achieved using relatively small doses of dilute bupivacaine, especially if administered in combination with intrathecal fentanyl. Ben-David and colleagues, for example, found that 3 ml of 0.17% bupivacaine in 2.66% dextrose plus 10 �g fentanyl intensified and prolonged sensory block for ambulatory arthroscopy without increasing motor block or delaying micturition and discharge [8].

Clearly, many questions remain unanswered about this neurologic phenomenon that is characterized by symptoms rather than objective findings. Indeed, the term previously applied to this entity—transient radicular irritation—may have been a misnomer because available data do not establish radicular irritation as the origin of these transient symptoms after spinal anesthesia. The relationship, if any, between local anesthesia, induced neurologic injury and pain or dysesthesia remains to be established. At this time there is no hard evidence to support the idea that TNS are on one side of a continuum leading to irreversible neurotoxicity.