Correspondence  |   February 2003
What Happened to the Paresthesia?
Author Affiliations & Notes
  • Christopher Carter, M.D.
  • *Anesthesia Services Medical Group, San Diego, California.
Article Information
Correspondence   |   February 2003
What Happened to the Paresthesia?
Anesthesiology 2 2003, Vol.98, 588. doi:0000542-200302000-00047
Anesthesiology 2 2003, Vol.98, 588. doi:0000542-200302000-00047
To the Editor:—
We read with great interest and enthusiasm the investigation by Urmey and Stanton 1 of the correlation (or lack of) between paresthesia and motor response during interscalene block. Unfortunately, a fundamental concept of their work was not addressed, discussed or, at worst, may be faulty. As a result, we are unsure how to apply their study and results to our clinical practices.
In the discussion, the authors state “the ability to elicit paresthesia in every patient in this study constituted evidence that nerve contact was made by the tip of the needle in every case.” They present no data or evidence to support this statement. We dispute whether paresthesia necessarily indicates needle contact with a nerve. As an anesthesia resident, I witnessed an open placement of an axillary catheter under local anesthesia. Each time the surgeon applied traction to a connective tissue septum within the neurovascular “sheath,” the patient experienced a mild median nerve paresthesia. Each time the paresthesia was produced, there were no instruments touching any nerves. Curiously, when the median nerve was retracted to allow passage of the plexus catheter, no paresthesia resulted. Finally, when the catheter was advanced within the neurovascular compartment, multiple median nerve paresthesias resulted. Clearly, paresthesia does not necessarily equal needle contact with nerve. In the absence of a clear understanding of the cause, or causes, of paresthesias, we find it difficult to interpret their results.
In our experience, most paresthesias are mild and immediately resolve in spite of the needle being immobile. The fact that the paresthesia resolves implies that “the event” that produced the paresthesia no longer exists in spite of the needle being “immobilized.” Taken further, many practitioners I know are reluctant to administer local anesthetic or choose to give a very small “test dose” in the setting of a persistent paresthesia for fear of an intraneural injection. Using this chain of logic, by the time Urmey and Stanton stimulated the needle, the conditions that produced the paresthesia no longer existed. In other words, the position of the needle relative to the nerve has changed. This alternative explanation is also consistent with their data showing that noninsulated needles produced motor response more frequently than insulated.
Finally, we tried to apply their study results to our own practice except we approached the problem from the other direction. We performed 19 consecutive interscalene blocks using a 22-gauge, insulated, short bevel needle and a nerve stimulator (Stimuplex Dig RC, B Braun, Bethlehem, PA). None of the patients received premedication. The stimulator current was set at 0.50 mA. None of the patients (0 of 19) experienced a paresthesia before a motor response was observed. All 19 blocks were successful (loss of deltoid/biceps and surgery performed without need for general anesthesia). We have a hard time understanding and explaining these data in light of the results and speculations by Urmey and Stanton.
Urmey WF, Stanton J: Inability to consistently elicit a motor response following sensory paresthesia during interscalene block administration. A nesthesiology 2002; 96: 552–4Urmey, WF Stanton, J