To the Editor:—
The article by Urmey and Stanton 1tested the hypothesis that if a needle should touch a nerve eliciting a paresthesia, an electrical current passing through that needle should also elicit a motor response. Since paresthesia was successfully elicited in 100% of cases but only 30% of patients exhibited any motor response to electrical stimulation up to 1 mA (200-μs pulse width), Drs. Urmey and Stanton seem to suggest that eliciting a motor response is unreliable, unnecessary, and may fail to signify proximity of the needle tip to the nerve. However, this conclusion is based on several assumptions, which deserve further comment.
The mechanism by which paresthesiae are elicited still remains the object of passionate debate. Paresthesia is a subjective symptom, which in many cases is difficult to differentiate from pain, and can be elicited by a variety of stimuli, including pressure rather than direct nerve contact. Although, we agree that eliciting a paresthesia suggests that the needle is producing some kind of mechanical stimulation of the nerve, the ability to elicit paresthesia in every patient does not constitute irrefutable evidence of direct nerve contact, and does not provide any insight on which part of the needle was involved in generating the paresthesia itself. This is a crucial point, because, on the contrary, nerve stimulation is mainly produced by the needle's tip. Rather than postulating a selective contact between the needle tip and a geographically isolated sensory component of the nerve (intriguing hypothesis but quite speculative), it seems equally plausible that the shaft of the needle, rather than the tip, was actually producing the mechanical stimulation. This hypothesis is also supported by the observation that associated motor responses occurred more frequently with noninsulated needles (in which the electrical field is also extended along the shaft). The observation that, once elicited, the motor responses were not related to the site of paresthesia further suggests that the shaft of the needle probably touched one nerve, while the needle's tip stimulated another nerve. However, it must also be considered that, though subtle, the withdrawal reaction upon eliciting a paresthesia may displace the needle tip from the position in which the paresthesia is obtained, and this may further affect the experimental model used by Drs. Urmey and Stanton.
The authors also suggest the high success rate of nerve block as an indirect evidence of the specificity of the paresthesia technique for nerve location. However, this result can be reasonably explained by the very large dose of local anesthetic administered (50 ml/750 mg mepivacaine). The relationship between the injected volume and success rate is well known. 2Excellent success rates with interscalene brachial plexus block have been reported with doses of local anesthetic ranging from 40 to 60% of those used by Urmey et al. 3–5Furthermore, the use of a low-current nerve stimulation (≥0.2 mA) technique as the primary method to localize the interscalene brachial plexus, results in a 95% success rate with only 35–40 ml of local anesthetic, even if no patient reports paresthesia in the brachial plexus distribution before or during motor stimulation. 6
Finally, although the authors carefully verified the output of the nerve stimulator before each use, the current intensity actually delivered to the patient was not measured. This is especially important when considering that the needles and nerve stimulator came from different manufacturers. The lack of an appropriate documentation of the actual current delivered to the patients may further affect the validity of the experimental model. Such caution is even reinforced when assuming, as stated by the authors, “the needle tip was in direct contact with a sensory nerve following the elicitation of a mechanical paresthesia.” Indeed, in this condition, the activation of the nerve stimulator should also result in an “electrical paresthesia” in the same distribution as the original “mechanical paresthesia,” especially considering the relatively high electrical energy applied (1-mA intensity with a 200-μs pulse width). 7However, this was likely not the case, as it was not reported. Using a low-power nerve stimulator, Smith and Allison 8reported that despite an often protracted search for paresthesiae, they were elicited in only 39% of cases, whereas the electrical paresthesia using nerve stimulation was obtained in all patients, and resulted in much higher success rates. Therefore, it is again extremely difficult to assume that indeed the needle inducing the paresthesia was directly contacting the nerve with its tip, raising one more time the question related to what paresthesia is.
In conclusion, while acknowledging the contribution of Drs. Urmey and Stanton in the still ongoing debate between the use of paresthesia or electrical stimulation for nerve location, we need data from studies using a similar design, but paying more attention to the definition of paresthesia, using lower volumes of local anesthetic and a well defined technique for nerve stimulation, as well as verifying that mechanical paresthesia would also result in electrically induced paresthesiae.
